Carbohydrate Health Concerns FA14

Carbohydrate Health Concerns FA14


[ Silence ]>>Hello there again. Excuse me, but there’s little
cake or icing or something in the corners of your mouth. Looks like you’ve
been eating some cake. I guess it’s a good
thing we’re going to talk about carbohydrate health
concerns in this lesson because it looks like
you need to be aware of what access carbohydrate
do, but also, some of the current
concerns that might come from carbohydrates not
being properly metabolized in that kind of bit. So, we were going to discuss
in this lesson and look at some health concerns that specifically deal
with carbohydrates. So, for basically diabetes and hypoglycemia is what
we’re going to discuss. But anyway, this graphic here
I’ve got just basically shows that anytime you
go to any extreme, either elevated blood glucose or
low blood glucose, that is going to be a health concern. So, we’ll discuss those and
see what we can enlighten you on as far as the nutrition
aspects of those diseases. But first thing I want to do though is just review a
little story I thought was kind of interesting, and it
kind of puts everything into perspective because– anyway, now, it’s just a
story it looks that, you know, how we should look at life. So, let me just read it to you and I hope we find it
interesting, so “The Difference Between Rich & Poor People”. One day, a father of a very
wealthy family took his son on a trip to the country
with the express purpose of showing him how
poor people live. They spent a couple of
days or nights on the farm of what would be considered
a very poor family. On the return from the trip, the father asked his
son, “How was the trip?” “It was great, dad.” “Did you see how
poor people lived?” the father asked. “Oh, yes.” said the son. “So tell me, what did
you learn from the trip?” asked the father. The son answered, “I saw that we
have one dog and they have four. We have a pool that reaches
to the middle of our garden and they have a creek
that has no end. We have imported
lanterns in our garden and they have the
stars at night. The patio reaches
to the front yard and they have the whole horizon. We have a small piece of land
to live on, and they have fields that go beyond our sight. We have servants who serve
us, but they serve others. We buy our food, but
they grow theirs. We have walls around our
property to protect us, they have friends
to protect them.” They boy’s father
was speechless. Then his son added,
“Thanks, dad, for showing me how poor we are.” Isn’t perspective
a wonderful thing, it makes you wonder what would
happen if we all gave thanks for everything we have
instead of worrying about what we don’t have. Appreciate every single thing
you have, things you see, friends and family and yourself. Life is too short. Enjoy the moment. I just thought that was a good
story, so I hope you enjoyed it. Anyway, we’re going to start
out looking at diabetes, and basically, diabetes
is a group of diseases that affect your
blood sugar levels. And so, it has to do with
looking at defective mechanisms that would keep your
blood sugar high. And so, that would be
called hyperglycemia. So what we’ll going to do
is just go through and look at the different aspects of
diabetes, look at the hormones that are involved, and look
at what some of the conditions that would occurred to being
diagnosed as being diabetic, and then in the end, look at
what we can do in nutrition– as far as nutrition aspects
of related to diabetes. So, I just want to
show you some graphics about how diabetes is a
growing disease in this country. You can see from ’94 to 2008
that the obesity has increased but also diabetes has
increased, so we’ll be looking at type 2 diabetes, which
basically is based on obesity. But the diabetes is a growing
concern in this country, but a lot of the type 2 comes from a growing concern
of obesity. So, we’ll be talking
about obesity later under energy concerns. Looking at Oregon specifically
because that’s where we live. We can see that diabetes
is going up to 2008. Now, you might ask why we
don’t have more recent data, and basically, they update
date about every 5 to 10 years. And so, maybe a few
more years before we get above 2008 and just in 2013. Anyway, the basic idea
is to look at the trend. The trend has been
going up since 1994 and is not increasing. Look at newly diagnosed
diabetics is really, again, the trend is to go up,
we had a big upswing in 2008 and till 2010. So– And I think it’s still–
I know it’s still rising. So, diabetes is still a concern. And then, the correlation
between obesity and diabetes is just
shown on this graphic. So, there’s a correlation there. And looking– excuse me. This thing is going crazy. Looking at Oregon obesity, I
just thought it was interesting to look at Hood River
County where I live close to versus Multnomah County and
there are the obesity rate. It’s kind of odd that
it is a lot different, so you’d think people
live about out in farming areas would
not be quite as obese as in Multnomah County, but that’s what this
statistic is saying. But we look at diabetes and you
can see that Hood River is lower but not too much than Multnomah
County and it is rising. So, these are just
some estimates of, you know, upwards of 67%. And then, there is an
ethnic basis for diabetes, the ethnicity does play a role. But again, you can
see the trends in all ethnicities are rising. So, it doesn’t really matter
the ethnicity, it just matters that the trend is
going up and up and up. And it doesn’t show
the Spanish population, but there is a high
incidence of diabetes within the Hispanic
population, Mexican, American or whatever population,
it is also very high. But this stuff is just
interesting, 50 fat diabetic, but ahead of you, but the
guy is doing the right thing. Part of the thing about
obesity is exercise. So, he’s doing the right thing. So, let’s look– pardon me, this thing just got
a mind on its own. So, let’s just look at the
regulation on blood glucose. Normal levels are between 70 and
100 milligrams per deciliter. It used to be not too long
ago, it used to be, you know, if you’re below 125,
you’re fine, but now, they’re diagnosing individuals
as prediabetic and trying to catch it before it actually
gets into the diabetes stage. So, the rule from now is
normal would be considered 70 to 100 milligrams per deciliter. But what this is
basically showing, the renal threshold is
basically the threshold where you’re not dumping sugar. And so, you wouldn’t have
glycosuria quite yet. But everybody’s level
is a little different. This is just kind of
an average level here. So, some people can be up
here, some can be lower. So again, it’s just
based on your kidneys and how much they
can hold back sugar and not dump it into your urine. But again, what we’re seeing, the normal trend would
be let’s just say, you started in between 80 and
100 there, the normal trend is after you eat food, then your
blood sugar level would go up. But then, insulin is going
to kick in and so forth and bring it back down. And then a normal level
would be to get down here and just kind of
go straight along. OK, what the extremes are
is if you eat, you know, especially carbohydrates and
your blood sugar level goes up but it just continues to go
up above the renal threshold and basically stays there. That would then classify
you being hyperglycemic, OK? But you can be hyperglycemic
without being diabetic. So, either some other symptoms
or hyperglycemia is one symptom. There are two other
symptom, basis symptoms that would be required for
you to be considered diabetic. But on the other extreme,
if it goes up, goes down and completely goes down, way
down, you know, below 50 and 40 in that range, you’d be
considered hypoglycemic which is another health concern
dealing with blood sugar levels. So, this is kind of the
scale that we’re looking at. So let’s first of all just
look at some of the hormones that are involved in
controlling blood sugar. And first one obvious and
you’ve probably heard a lot about it is insulin. So, insulin is made by the
beta cells of the pancreas. Its main job is to be a produced when blood sugar
levels are high. Actually, insulin is produced
before your blood sugar levels gets high, because as you
remember from the regulation, we have the biggest nerve
that basically so going to tell all your body parts
when things are being eaten and to prepare to receive food. So, insulin is actually
going to be prepared and made before the sugar
actually gets to the blood. But it’s going to
be made in response to a potential glucose
absorption and increasing blood
sugar levels. It also has a feedback
where it’s going to prevent the glycogen in
the liver from being broken down into glucose and then you
put it into the bloodstream. So basically, you know, the
feedback system was there, “Hey, we’re going to get some glucose
coming in, so there’s no reason for you to puddle
me in to the blood. So, we’re going to stop
breaking down your glycogen and you can just keep it.” It also is going to have an
affect of increasing the stores of glycogen in the liver
if the liver is on full. I mean, there’s a limit
to how much glycogen that liver can hold if you
go over that limit and go over the limit that goes
into the muscles, then, it’s going to go into
adipose tissue and become fat. But– And then also are
it prevents fat breakdown which basically is one of the
premises of the Atkins diet. The Atkins diet as you
know is low carbohydrates. So, the basis of that would be if you’re eating low
carbohydrate, you’re not going to produce insulin,
therefore, you’re not going to prevent that breakdown. Therefore, your body would use
more fat as an energy source. Problem with that is it’s
going to go into key tones and you get into ketosis. In long term, that’s
not a good thing to be in ketosis for a long term. Very effective, acting
size is losing weight fast but it’s not a long term
solution, it’s not one that you’d want to live up
for the rest of your life. So anyway, so this is kind
of the effects of insulin. Insulin comes from the pancreas and the pancreas is right behind
the stomach here, is going to– so the pancreas is
pretty important, it’s an exocrine gland as
well as endocrine gland, because we talked about the
pancreas when we’re talking about digestion as making
lipases and proteases and those kinds of things. And so, they’re going to go–
they’re an exocrine so they go through a duct that
would go to the duodenum. But it’s also an endocrine gland
that’s going to secrete insulin or the hormones right
directly into the bloodstream. So, it’s a pretty important
organ, but in for our case, we’re talking about it’s
relationship to insulin. The main part is the islet of
Langerhans, and you can see, here are the beta cells
as part of that process. We’ll be talking about alpha
cells also here in a minute, but the beta cells are
going to produce the insulin that are going to be secreted
out into the bloodstream. Now, a lot of students think
that insulin is going to grab on the sugar and bring
it into the cells. Actually, insulin is a hormone and hormones tell
cells what to do. In this case, insulin
is going to fit in to the insulin receptor,
and it’s going to send a bunch of signals to produce
glucose transporters. And so, these are
going to be, you know, if you got 112 hopefully,
these are going to be active transporters
that are going to basically transport
the glucose from the bloodstream
into the cell. And they do have names and I’ll
show you some later like GLUT4, GLUT1, GLUT2, those kinds
of things as depending on what cell they’re part of, but the GLUT part is an
indicator that is going to transport glucose,
OK, in this case. The next thing that’s going to
happen is that– back up, OK? I got frustrated
because it went on. But this is just
another illustration of where insulin is going
to work where it fits in to the insulin receptor and basically then goes
throughout the process of producing an active
transporter that’s going to take glucose, bring
it in, and eventually, either this is going to be
put together to make glycogen. So, this would be in the
liver or in the muscles, not– so this wouldn’t necessarily
be part of adipose tissue. But there will be part of
either the liver or the muscles. So, here’s just an
example for you. I don’t expect you
to remember these and where they’re distributed. I just wanted you to know that
they do have names depending on what tissue they are part of. GLUT4, they were just looking
at it as part of skeletal tissue and cardiac and that kind of. GLUT3 is in your nervous
system and other places. GLUT2 is going to also be in the
liver and that kind of thing. So, it just depends
on where it is. But all of them are going to be
glucose transport proteins, OK? I keep hesitating
because I don’t want to see what’s going to go out. Anyway, so that’s
basically insulin. Amylin is co-secreted
with insulin, it comes from beta cells also. And it has three things
that I’d like to remember about amylin is going to
suppress glucagon secretion. And glucagon is we’re
going to see in the next– as part of the next
hormone basically is going to tell the liver to
produce, you know, to break off the
sugars from the glycogen and send them out to the blood. So, if we suppress that hormone,
it’s not going to be able to tell the liver to
do that, so very cyclic and you keep the
glycogen in the liver and not increase liver
secretion of glucose. It’s also going to basically
make you feel less hungry, so you don’t eat. That’s one of the feedback
mechanisms, amylin is. That is going to
make you feel fuller and that’s what satiety means. Satiety means a feeling
of fullness. So, that’s just one of
the feedback mechanisms that just basically
going to tell you, “Hey, you’re getting enough to eat,
we’re getting plenty here so you can slow down
and stop eating.” It doesn’t mean we
are as we’ll see later in one of the other lessons. But it just means that
in reality, we feel full. But if we see dessert, we’re
going to still eat it probably. So, here’s the amylin that
is going to be secreted again from the cells of the pancreas. It’s going to go to the liver
and basically do the things that we just talked about. So, it’s co-secreted
with insulin. I’m going to keep my hands on
both of this in case it bump. Here, I just talked
about glucagon, it’s produced by
the alpha cells. So earlier, I showed you
that the beta cells are in the islets of Langerhans. But the alpha cells are going
to produce the glucagon. And it’s in response
to low blood sugar. So, insulin and amylin
would be involved when your blood sugar
levels are high. Glucagon is going to be involved when your blood sugar
levels are low. So, you would see production
of insulin and amylin after you’ve eaten something,
you would see production of glucagon whenever your
blood sugar gets low. For example, when
you’re sleeping at night or you are attending to
get more hypoglycemic if you haven’t eaten for a while and your blood sugar
level stores, blood sugar levels go down, then those blood sugar levels
are going to be brought back up to homeostasis by the
production of glucagon which will tell the liver to
break off sugar from glycogen and put it out into the blood. So therefore, that’s why it’s
stimulating the liver glucose to release glucose and helps to
basically maintain homeostasis of your blood sugar levels
during the fasting period which will be like when
you’re sleeping at night. And so, here’s just
some example. Here’s glucagon and then it’s
going to go about the process of taking glycogen,
making glucose and then that glucose is going to be
secreted out in the bloodstream because of glucose levels
in the bloodstream, OK? GLP-1 is kind of a neuron,
it’s an interesting one, it secreted not from the
pancreas but from the cells of the intestinal track. And so, it’s going to
be basically stimulated when you have food in
your intestinal track. So, not necessarily
in the bloodstream. So when the things get into the
intestinal track, the duodenum and so forth, then the GLP-1
is going to be produce. It’s going to then do
a positive feedback to cause insulin to be secreted. Then, it’s going to also help
amylins suppress glucagon, it’s going to help with amylin
to make you feel satiety. It is– The stimulation
of this is actually going to increase amount of beta
cells and increases beta mass. It actually helps keep
the quantity of beta cells within the pancreas,
so that’s stimulation. So what they found is, if GLP
is one and GLP-1 is not working, it’s not being secreted because
you have some defect, then, the beta is so mass actually
starts going down and down because it is not
being stimulated. It’d be similar to
your muscles shrinking because you’re not working out,
you’re not working your muscles or your bones get thinner
when they’re in a cast after you broken the bone
and you don’t walk on it for a while, your
bone mass gets smaller because it’s not being used. Well basically, the GLP-1
will stimulate the beta cells in active and keep them
dividing and so forth. And also, it helps through
efficiency, so that’s good. So, GLP-1 here is coming
from the intestines that goes to the pancreas and then
stimulates things to beta cells and so forth in the
pancreas, OK? Epinephrine is one
that is produced during fight-or-flight mechanisms. So, when you’re under stress,
do you’re fight-or-flight, then adrenaline is meant
to utilize more glucose. So, you can make more ATP
so you can have more energy, they’re run or fight or
whatever you’re going to do. The problem is and we’ll talk
a little bit more about this when we get into hypoglycemia,
I mean, the initial response is to increase blood sugar, but
also their response is going to be to produce more ATP. And, you know, your nervous
system is going just crazy like this. Where it can come into play
with hypoglycemia is because if, you’re under constant stress
or fear or you’re afraid or your stress because you’re
afraid of something or nervous or you’re just fearful
all the time. You can’t sleep,
you can’t do things. And maybe who knows you got a
restraining order at somebody or something and you are
just nervous all the time or you got a nutrition test
coming up and you’re just stress about your nutrition test or– but this would be
stress that goes on 24/7. The fight-or-flight
stress is supposed to be for very short period of time, just enough energy
to get you going. But if you’re under
fear 24/7, you’re going to be producing a
ton of epinephrine. Your nervous system is
going to be going 24/7, you can bring your blood
glucose levels too low because you’re just
under that stress and you’re just trying producing
ATP and you’re under anxiety and you’re going nuts. That can happen. So we’ll bring that up again,
but again, what we’ll talking about it here is
because it is a hormone that can affect your
blood glucose levels. OK. And so, here’s epinephrine
that would be the same as glucagon but it’s
going to cause glycogen to produce glucose and then fuel
that for fight-or-flight, OK? So, we’ll talk more about
it epinephrine adrenaline. So, let’s look at the
clinical manifestation. Basically, this would be
what would diagnose you as being a diabetic or in
this case a prediabetic. So, prediabetes would
be if you– a fasting glucose would be
if you fasted for like 10 to 14 hours and then
had a blood test. So, it would be around
in the 100 to 125 range or if you had a glucose
tolerance where, and I’ll show you
picture in a minute, where you would have a
glucose tolerance test where they’d give you this
really seeking sugary stuff and then they would takes
blood samples and monitor how– if your glucose goes up and
then if it comes back down. If it goes up and
stays up into the 140 to 199 milligram per
deciliter range, then, you would be considered
to be prediabetic. And so, they just recently
been using as a diagnosis because they will look at this
and look at trends because, you know, you start
out and they– you’re maybe at 105 and they
say, “Well, you are getting into the prediabetic range.” And then the next time you
go back to doctor to 115 and then 120, so
they’re noticing a trend. And in some cases, they may
prescribe insulin even though you’re a prediabetic or some
kind of a therapy because your– because they don’t want it
to get to the 125 range. They don’t want it to
get to the 200 range. They want to catch it
before it gets there, before it can start causing
some of the physical problems that we’ll talk about
just in a minute. So, prediabetes is now a
diagnosis, it would be something that you’d find in
a patient’s chart, and it would be again
looking at, OK, we’re in the prediabetic,
we need to start looking and doing something so it doesn’t continue
to trend upwards. Now through diabetic,
you’d be over 125 fasting and 200 blood glucose,
but it also one thing that they are also
looking at, you may or may not have heard
of the A1C test. I mean the official name is
glycosylated hemoglobin A1C. But usually if you work in a
hospital, they will just say, “What is their A1C levels?” because that [inaudible]
that means. And we’re looking at– and
I’ll show a little diagram that shows what does
7% glycosylated hemoglobin represent. But let’s just talk a
little bit about for second after we get through this. So, here’s that glucose
tolerance test where they give somebody a sicky
thing and then they would– our glucose and they would
basically just monitor blood glucose levels. If you’re normal, it would go
up obviously and then come back down and kind of level out. If you’re diabetic, it’s going
to have way up here and that’s where you would be classified
as hyperglycemic, OK? So, hyperglycemia is one
indicator of diabetes. You can be hyperglycemic but not
have the symptoms of diabetes, still, you have high
blood sugar. But it is waves of red flag. So, there are two other
things that are going to be manifestations that
would clinically diagnose, she was being a diabetic. So, we’ll talk about
those in a minute. But let’s look at the
A1C and what it means. Basically if you haven’t
had anatomy or if you have, you should know that red blood
cells live about a 120 days. After about 120 days, they’re
going to be broken down and, you know, everything is going
to be kind of reused for that. So, the A1C level is a diagnosis that would tell you what is
happening over a 121-day period or a three month period, OK? So, it can tell you how things
have been going on average for the last three months
as opposed to a finger stick which basically tells you
at the moment or a serious of putting your sticks that
may not be as accurate. This tells you an average
because what happens is that overtime, depending on your
blood glucose level, I mean, your glucose will bind
to red blood cells. But the higher the
level of glucose, the more glucose is going
to bind per hemoglobin. And so, if you have
hope low blood glucose, not as much sugar will
bind to the red blood cell. If you have high
glucose, more will bind. And so, they call
that glycohemoglobin but the test just the A1C. So basically, this is the idea. At a low A1C, you see you just
have a few sugars attached to the hemoglobin and
the red blood cell. Here, you have more. So, this would be a high A1C
levels because you have a lot of sugar that is attach
to red blood cells. And so this would
be an indicator of how your sugar levels have
been over a three month period. It used to be a good test for to see your patients were
actually telling you the truth because they would come
in with finger stick. And I hope you know
what a finger sticks where you poke your finger
and you have that little thing to advertise on TV that
takes your blood sugar level. And so usually, you
know, for new diabetics, they have you do it a
couple of times a day or even once before eating, once
after eating kind of a thing. And so, a lot of times patients
would not tell the truth because they didn’t
want to be in trouble and they didn’t wanted,
you know, they only want the doctor
think they’re doing a good job. But then, they would have
low blood stick, you know, finger stick levels and then
they would look at there A1C and it’s really high, so they
knew something was goofy there. And so, there glycosylated
hemoglobin, the A1C is a more
trustworthy test than the finger sticks
basically are. So, here’s the A1C scores
and you can see, you know, seven is good, you know, within
this range if you’re a diabetic. You know, if you’re
not diabetic, you know, obviously you want
it below that. You know, obviously you
want to be in the five range if you could between
five and six because that basically indicates
that you are in, you know, below the hundred range. But for a diabetic who’s
really struggling to control, they feel that a
seven is a good– pretty good number
if they can maintain that over a three month period. Because you’re blood sugar is
going to go up and down and up and down and up and
down, you know, everyday. But if you can average seven,
you know, about a 150, you know, for diabetic, they’re figuring
that that’s a pretty good number that they can be comfortable
with, that they can stay with that because
it’s not extremely, it’s not a real high
levels that you can get to. Anyway– And, you know,
hyperglycemia, you know, it looks like 380, I
mean, that’s really high. It is not uncommon for
undiagnosed diabetic to come into the emergency room with
diagnosis of blood sugars of 500 to 700 something like that, because they didn’t
know they were diabetic and they were eating just
tons of food in terms of carbohydrates and stuff,
and then all of a sudden, they just feel goofy and
they feel a little weird. And so, they go to the
emergency room and get tested and there you are, you’re in
a 500 to 700 kind of thing. OK. The second thing that would
be a clinical manifestation that they would look at to
give you a full diagnosis of diabetes would
be keto-acidosis, diabetic keto-acidosis. Basically, when your cells
aren’t getting glucose, they have to get
energies from somewhere. And so, that energy tends
to come from abnormal or inefficient breakdown
of fatty acids. And those fatty acid
would then become ketones. Well, ketones are
basically acidic. And so, you’re going to be
acidifying your blood and go into what can become ketosis. So if– they can also do a test where they can test
your ketone levels and basically they
can tell, you know, that would be another
diagnosis that your, you know, you have hyperglycemia. But are your cells
not getting sugar? OK? Because you can be
hyperglycemic, again, you blood– your cells
couldn’t get in sugar, so they’re not burning fat. But another indicator that
you’re not utilizing the glucose and it’s high in you’re
blood would be to see if you’re having– if your
body is having to make ketones in order to get the
cell’s energy. And so if you ketone levels are
high, then you would know, yes, you are having to make ketones. So basically, ketones come
from, you know, with you– hopefully if your taking
112 and you’ve looked it in the respiration we
talked about acetyl-CoA. And so, and if you remember
fatty acids can only be broken down if they go into the
mitochondria into acetyl-CoA. Remember, they’re broken down
into two carbon units that go into the mitochondria
become acetyl-CoA, then, they can go to the Kreb cycle
electron transport chain and become energy. But in this case, then, what
you’re going to be making is, you know, you’re going to
make a lot of acetyl-CoA. But some of it, you know,
is going to become ketones or acetones and those kind
of things, which then can be, you know, build up
in your bloodstream and cause ketoacidosis. So, here’s another,
you know, inefficient or absent insulin basically. You’re going to be
creating this, you know, ketogenesis where
you’re going to– neo means no, basically none, so you don’t have any
genesis of glucose. So, you’re making ketones, you
increase ketones in the blood. And basically, you know,
what this is saying is that, you know, if you look
at this whole scheme where it says increase
ketones and glucose, basically, what’s going to happen
is the cells are going to be signaling the liver
saying basically, “Hey, we must be in hypoglycemia because we aren’t
getting any glucose. There’s no glucose. And so, I think you
should release more glucose because we’re in hypoglycemia
even though your bloods actually in hyperglycemia.” So, the liver can
break off sugars and put them into the blood. You know, when your diabetic
increasing your blood sugar level is even more. So, you can even become
more hyperglycemic because your bodies responses,
“Hey, we don’t have enough sugar in the blood because our
cells are not getting any. So, please give– put
some more in there so there would be
some more available.” But it’s not going to be used. So, you can become even more
hyperglycemic but you’d also– the cells were saying, “Well,
we’re not eating glucose, so let’s try some thing else. Let’s work on getting
some ketones here.” And so, you’re going to break
down fat and you’re going to increase the amount
of ketones. So, you can become more
hyperglycemic and, you know, more ketone, you
know, bodies basically in your bloodstream that way. And the third one would
be if you have glycosuria which basically means you’ve
gone over the renal threshold and your dumping sugar
into your urine, OK? What that can cause is obviously
polyuria and I can’t remember if I have may have a little shot
after this, I can’t remember which slide comes next. But anyway, we talked a
little bit about this in BI12 or if you took another
biology class when your talking about osmosis and
diffusion, we basically said if you have high glucose
in you’re blood basically, that makes your blood
hyperglycemic, therefore, you are going to have
more water in your cells in the interstitial fluids
than you do in the blood which is basically going
to cause water to move into your bloodstream. Therefore, the high water
is going to cause you to have polyuria, so
increase urination. Then, you’re also going to be
very thirsty because, you know, you’re urinating a lot,
you’re taking away, you know, fluids and your body responses,
“Hey, let’s drink some more because were losing
a lot of fluids.” And then, you’re going
to be very hungry because your cells
aren’t getting glucose. And so, they’re sending
signals, “Hey, feed us. Feed us. Feed us. We need more carbohydrates.” And, you know, so not only
they’re telling the kidney to send signals, but with
this, you know, to send glucose to the blood, that they’re
telling your body, you know, “Hey, feel hungry because
we need to get this guy to eat something because
we’re low in glucose here.” And then because you’re
not getting any glucose, I mean, you are burning fats. And so, you do get
weight loss but also a lot of the energy, you know. The glucose that would
be going into the cells and also maintaining your weight
was going to go down the drain, so lot of signals there. So, hyperglycemia diabetic
ketoacidosis, so ketone low and glycosuria would
be the three main test that they would do that would
give you a full diagnosis of being a diabetic, OK? What are the complications
of diabetes? Number one, here are the risks. You can see the risk
go very high. Cardiovascular disease
there’s an increase, you know, 400 times increase in cardiovascular
disease with diabetics. And then, you know, strokes because of high blood
pressure that’s going to be caused and
things like that. So, a lot of emphasis to get
your blood sugar into control, whatever means it takes. This is just looking
at renal disease. Some of you are going
to be working in a renal units were
they do a lot of dialysis. High percentage of those
patients will have had diabetes because it is going to
basically destroy nephrons and parts of the glomerulus. And so, I have this
little blurred that I got that talks about podos. Ihave never really heard about
podocytes before I found this. But these are part cell,
basically part of the glomerulus which is a filtering
mechanism within the kidney, and basically, they don’t have
receptors, so they’re going to be impaired and so they
result in abnormalities. And then also, that
lack of insulin is going to affect the cytoskeleton
for whatever reason and the structure of that. So, it’s going to basically
damage the kidneys through that. And so, that’s where
you get in nephropathy. But here as I just– I found
a picture of podocytes. And so, basically if you
don’t know the glomerulus, the blood comes in and
goes through these series of capillaries that have holes
in them and the back pressure because this tube is
smaller than this one. So, the blood can’t leave
as fast as it comes in. It will probably cause pressure,
pressuring things to be filtered out into this– used to be
called Bowman’s capsule, now they call it the
glomerular capsule. But here, just the filtrate
would be water and urea and different things
but also sugar. And then, it does
down these tubules that will become
part of the nephron. While here, the podocytes and apparently it causes this
structure to become defective. So, you can’t filter things. And so basically, it ruins
the ability to make urine. And so, it results
in nephropathy which means you can’t filter
your blood without going to a dialysis in either
something like that. And so, macular degeneration because you increase
hypertonicity of your blood vessels going
through your eye basically, and it can cause hemorrhaging,
it can cause aneurysms, you get high blood
pressure in those areas. And so, it can cause
some retinopathy to occur as part as being diabetic. So, that’s a problem there too. The other thing about where it
can cause is getting numbness because of lack of–
if you think about it, if you have high sugar in your
blood, it becomes very syrupy. I should have brought
out my little sticks but I don’t think you could
see them on the screen. But basically, your blood
becomes more like syrup. And so, it flows a lot slower
which is why you may have heard that diabetics have to
really watch their feet to make sure they don’t
injure their feet. So, if they have any kind
of injury on their feet, it’s very difficult
to heal that sore. Because number one, it takes
more time for your immune system and stuff– white blood cells
and stuff to get to the wound because your blood is syrupy. But also, the bacteria
love your sweet blood. They’re going to grow very
rapidly with all the sugar in your blood and
that kind of thing. So, diabetics really have to
monitor their feet and make sure that there’s no sores
down there. If there are, they need to go
to a podiatrist or to a doctor and get them, you know,
analyzed and make sure that they’re taken
cared of properly. But the other thing about it
is that they can get numbing in the feet, numbing
in the fingers as part of the nervous system being
affected by the bloodstream. And so, it sometimes can– if
you have numbing in the feet, it can be difficult
to feel if you step on something sharp or something. And so, you could
get a sore down there without even knowing it, which is again why they
recommend diabetics and, you know, especially, you know,
when you take your socks off, then you inspect your feet
and make sure that there’s– that there are no
problems down there. OK. Corns can be a real
issue with diabetics, having them taken off. So, you really need a
professional to do that. You wouldn’t buy off the
counter thing to take off corns. You would want to go to
a podiatrist or a doctor and get them really
taken cared of properly. OK. So needless to say, diabetes
has a lot of side effects. Let’s go over the
classifications. Type one, type one is basically
the lowest level of diabetes. There’s only maybe the– I mean,
the range they give is 5 to 10% of all diabetics or type one. It seems kind of a wide range,
but it’s within that range. It’s an immune system problem. It’s not really a diet problem
and that’s what I need you to understand is that in most
cases, type one is not caused by something nutritional. It’s an immune system problem. It’s a very– a brittle– it’s called brittle because
it’s fast acting rapid because it can happen
over night. One day you feel
like you’re normal, next day you’re not normal. It’s just almost
happens over night. Very rapid. It’s very brittle because it’s
very hard to control some thing. When you first start
trying to control it, then, it gets very hard
to get it nailed down to how much insulin
do you need, you know, that kind of thing
versus, you know, your insulin food intake
are kind of balance. So, it’s kind of
hard to balance that. It can go up and
down and up and down. One day and the doctor is fine,
next day it’s really high. Come in the doctor’s
its really low. And so, they’re always
monitoring which is very frustrating when
you’re a diabetic especially if your– because type one
usually occurs in early life. If you’re a teenager
or something that’s– its very difficult because,
you know, your life is just put into a whirlwind, you
know, your sugar is up and down and up and down. And I mean, your hormones
are raging and you’re in that decade, you
know, where, you know, just a lot of things are
happening in your life and then this happens, and
if things going up and down and you want to get in control
and it doesn’t get in control and your just, you know, it’s an
emotional drain, very stressful which is why a lot of times
type one teenagers are ones that don’t follow diets. I mean, they just don’t want to. They’re upset, they’re
mad, they’re angry because they’ve got
this diabetes. And they can’t do
what their friends do. They can’t just go
out for pizza. They have to watch–
They have to take shots and they don’t want
their friends to know. And so, they go into
the bathroom in secret and take a shot. And just stuff, it’s
just all kinds of stuff. So, it can be very brittle,
a very hard to control, which becomes very,
very frustrating. It’s an autoimmune
which basically means that your body is
attacking itself. And it’s going to destroy beta
cells therefore reducing beta cell mass and reducing the
amount of insulin to the level where you don’t produce
any insulin at all. But again, no nutritional
cause, it’s not caused by eating too much sugar. It’s not caused by eating
too much carbohydrate. It’s not caused by obesity. It’s caused because
of your immune system, something’s going on. OK, well, what causes your
immune system to attack itself? Well, what they find is
that there are some people who are just genetically
prone, they’re genetics in such that they are more prone to immune system
attacking the beta cells. But what they found is it
takes a stressor to do that and the stressor
can be, you know, you don’t even have the
symptoms of type one. Then, you have a fever
or, you know, real sick is when your fever gets real high. And then all of a sudden in a
short period of time after that, you find out you have diabetes
o a heavy stress or, you know, hormone changes or something. Other people what they found is that viruses will
attack the beta cells. And again these individuals
are genetically prone for some reason to receive
these viruses and they’re able to get into the beta cells. Well, the body’s
response is, “Hey, I need to get rid of that virus. The only way I can do it
is to destroy this out. And so, your body
attacks itself. And so, they can test, you know,
test for type one by testing for antibodies that
are being produced. And these are some of the ones
that they could check to see if yes it is indeed type one because you’re producing
these antibodies that are autoimmune
antibodies to your system, OK? So, that’s the issue there. And again, what’s its going
to do is if you lack insulin, you are not going to be
producing the transporters. Therefore, you cannot get
the sugar out of your blood. So, the obvious thing
that you would have to do is take insulin injections
in order to have that insulin to make the transporters. OK? And so, this is
just another figure that says basically
the same thing. If you have diminished insulin,
you don’t have the signals to make in this case
the GLUT4 transporters. You do still have some
glucose transporters but it’s very diminished and
you just can’t get all the blood out. So, you continue to
be hyperglycemic. All right. Type 2 is a different story. It has to do mainly
with insulin-resistance. It’s used to be called adult
onset, but we’re finding more and more individuals
in the adolescent age that are getting type 2. We’re seeing more and more and
we are seeing a high increase of individuals in the
age range of about 35 that are getting type 2. It used to be– it was in maybe
your late 40’s or in your 50’s where you would see type 2. And a lot of it had to do
possibly with the fact that, you know, you’ve been
overusing your pancreas. Something happens with
the pancreas or something. Or, you know, your
cells just get tired and get resistant something. But this indicator is really in, as we’ll see, because
of obesity. It is a progressive
loss of beta cells. Type 2 can eventually become
type 1 if it is not taken care of because there will be over
time a loss of beta cells. So, you start decreasing. Initially, type 2
is not a problem with production of insulin. You produce plenty
of insulin which– so which sometimes it’s called
non-insulin dependent diabetes where you don’t really
need insulin because you’re producing
plenty of insulin. The problem is it’s
not being able to– the cells aren’t
responding to it, so they make the transporters. So the same condition
is going to come about is you’re not
making transporters. It’s just in the case of type 1,
you’re not making the insulin. In type 2, the cells don’t
respond to the insulin. So something is happening with
the receptors or, you know, the not– maybe not necessarily
has to be the receptors. It could be the receptors
aren’t sending signal or they maybe sending a signal
but it’s not being responded to and we would call that
post receptor defects after the receptors. So, we’ll talk about those. I wanted to bring up
gestational diabetes because what they found is
that there’s a higher risk of women getting type 2 diabetes if they have had gestational
diabetes during pregnancy. And so, gestational
diabetes is diabetes that only manifests
itself during pregnancy. And so, there are
some theories on why. They have found some
decrease in GLP-1. So, it’s not stimulating
the production of insulin during pregnancy because of hormones
that do that. And then, there’s
some indications that amylin could decrease
or maybe be resistant that isn’t it just
not working properly. So, that could lead
to the diabetes. Because lot of cases,
once pregnancy is over and delivery is over, then,
the diabetes goes away. But what they found is
it should wave a red flag to those individuals who
have had gestational diabetes that I am at risk, a higher
risk than the normal population or I shouldn’t say normal
but the other individuals who haven’t had gestational
diabetes to getting type 2. Because there are
individuals who are obese who don’t have type 2. But these individuals
would be at higher risk that if they got– that
if they became obese that they would get type 2. So, it’s just a red
flag that’s been raised. So, what does obesity do? The main obesity that is the
problem and we’ll bring this up later and later
in heart disease, in cancer everything else
is visceral or central. This would be obesity that is where you have fat underneath
the rectus abdominis, the muscle is here, so it
would be underneath that layer that is going to
push the muscles out. So, this would be individuals that have very hard
stomach but it sticks out. It’s not the jelly, jiggly
santa clause fat, it’s the fat that is very hard and sticks
out because it’s pushing against the muscle layer. This is the worse fat
that you can have. I may have mentioned it before but I’m just going
emphasize that, again, that this is the worse
fat you can have, mainly, it’s called visceral. It’s not really– I mean, sometimes some people
may use abdominal obese but you can have
subcutaneous obesity which is the giggly stuff
on the outside of the muscle that would be in the abdomen. So, it’s more better fuel to
be called visceral obesity because it surround your
intestines and your visceral. But what visceral obesity
can do is it can result in insulin resistance
which basically means that you’re going to have
faulty insulin receptors. So, the receptors are going
to be made in correctly. And then, so the
insulin doesn’t fit. Remember from biology, we said that these receptors
are protein, and if they’re not made
correctly, then, the insulin, you know, things
won’t fit in there. Postreceptor defects we guys
are talking about, meaning, that maybe the receptors
are find, they get– they receive the insulin,
the insulin fits to receptors and starts the signal process. But in the process of relaying
the signal to the nucleus and so forth, something
gets screwed up. So, that would be after
the receptor, postreceptor and this would be part
of the relayed protein. Some of you that had my
biology class, remember, we talked about relayed
proteins, when we talk about cancer, and we
talked about the ras protein with signal, the
tyrosine-kinase. And we’d have this 35 proteins
on the way that nucleus. These relayed proteins could
be part of the factor process. But any sense there, the signal
is not getting to the nucleus, so the nucleus can send
the information and go to transcription translation
to make the transporters and through the ribosome and
the rough ER and all that stuff that you should have
learn and, you know, embed them into the plasma
membrane to take the sugar out, So this just not happen. If you have been
obese for a long time, you are basically
running your pancreas at 100 miles an hour,
you know, max. There can be a point
where your pancreas says, “Enough is enough. I give.” And it starts– your
beta cells start dying off. And so, you decrease
your beta cell mass. So in these instance, it’s
called pancreatic exhaustion. It has to do with obesity
but it doesn’t deal with how obese you are, it deals with how long you
have been obese. So, it’s about length thing
versus, you know, how big of– you know, how much
obesity you have. So it’s the length. And so overtime, you’re
just overtaxing the kidney or your pancreas. Your pancreas gets exhausted
and says, “I give,” OK? And just throws in
waves or white flag, throws into [inaudible]
and then going to be made. There is another
theory basically that and it’s hard to explain. Let me explain with my hands. But it kind of visualize
that you have this cell and you have these receptors,
and kind of visualize because it’s a little
bit, you know, receptors are a little bit more
complicated than we make it. But let’s just visualize
that it takes two receptors to receive the insulin. And so, the distance of these
receptors apart is significant because the insulin has to fit
into both of those receptors. So, as you get obese, your adipose cell size
the cells get bigger. So the theory would be
that the two receptors as– it’s kind of a like blowing up
a Mickey Mouse balloon, right? So, the faces are all
crunched up and then, you know, it going to widens up and
the ears get farther apart. Well, these receptors are
going to get further apart as the cell gets
bigger, they’re going to be squeezed further
and further apart. Well, if the insulin
is only this big, it can only fit one part
of it into one receptor, the other receptors
weigh over here. And so, the insulin is in
effective because it don’t fit– don’t fit?– doesn’t fit, OK? But a lot of times, you
can– if you lose weight, you will not be type 2,
you will not be diabetic, you can control it with weight. So, the theory would be
that as you lose weight and your cell size gets smaller, the two receptors become
closer together again, and so the insulin will fit. Kind of a theory, it’s
called the fat cell theory or adipose cell sized theory. You know, it may have
some there but who knows. But anyway, these are some of
the things that would cause– would be caused because
of visceral obesity and that kind of thing. But we’re going to talk more
when we get to heart disease. But in this instance, visceral
obesity and I– we think– you probably have heard that
fat cell send out signals. They are not just storage
vesicles, they actually send out signals that are going to
cause things like inflammation or they can cause, you know,
havoc with some of your cells. And especially because they
are visceral, they go directly into the blood and go directly
to the liver and then directly to your cells, and they
can cause more havoc. So, let me just go
through a scenario to try to help you understand why
obesity would cause type 2 diabetes. And this is just an illustration
basically that, here, the insulin– you have
plenty of insulin. The insulin fits your
receptors, but there’s a defect in the signaling somewhere. So, the information doesn’t
get into the nucleus, the transporters don’t get
made basically, and so, you don’t going to include those
in, and so they just don’t work. So that would be a post
receptor type of defect or they would call it
insulin resistance. That’d be one type. So, here’s the picture
with the obesity. It says the developing
pictures that free, so FFA’s are free fatty acid
which basically means, you know, from a triglyceride, you
have the free fatty acids and are going to enhance
the secretion in obesity and sooner resistance
syndromes, OK? And so, it could contribute
to beta cell failure and development of
type 2 diabetes. And this is going to
be especially important with visceral obesity
releasing these free fatty acids into the bloodstream, OK? So, here’s kind of the idea is
that when you start breaking down fat– visceral fat, it
seems to be the one that some of you may know if you
tried weight loss is that the subcutaneous
is the hardest to lose. The visceral is the fat
that’s going to be used first. So even though your stomach
will go down because of lack of visceral, you may feel– look like fat because your
subcutaneous takes longer because the visceral is
going to be used first. Well, if the visceral
is used first, then, it’s going to produce, you
know, the lipids that are going to become the free fatty acids. The key is again, oxidation. We talked about oxidation
earlier. So, these free fatty
acids can become oxidized, they can decrease
glucose utilization, increase glucose neogenesis and then you’re going
to get hyperglycemia. So, the cells will
not take up glucose. The liver will produce more
glucose, so neo means new so new glucose genesis
or production. And you’re going to become
hyperglycemic that way. The other mechanism again,
looking at insulin resistance, you’re going to increase
lipolysis, increase plasma in the blood, free fatty acids. This is tumor necrosis factor
that can cause inflammation which is another
problem and then– but, you know, the ultimate
result is that you’re going to become hyperglycemic
by reduced plasma insulin, decrease glucose or
increase glucose output because the liver, the
cells are going to say, “Hey, we’re hypoglycemic.” And then, decrease in
glucose transporters. So, all of that is
going to be happening because of the breakdown
of visceral fat. It seems to always
go to the next frame when you have these
circles that I’ve done. Anyway, here’s another
scenario is that here’s stresses from obesity and stresses can– because of the tumor grows this
factor that cause inflammation, because of excess free
fatty acids that are coming from the breakdown
of visceral fat. And so, these would be
called stressors, OK, because they’re going
to stress the cells. They’re going to get in, they’re
basically going to stress. Here’s the endoplasmic
reticulum basically the rough and it’s going to cause
unfolding of the proteins. Remember, the folding
of the tertiary and secondary structure
of the proteins. And so, then basically
the long term it’s going to inactivate this and you’re
not going to make the glucose or the glut transporters, OK? So, the visceral obesity,
the more you have, the more you’re going to use
it, is going to cause stresses and is going to result
in lack of transporters which therefore we would
call insulin resistance, OK? So, anyway, there is
a type 1.5, there– it’s called by many different
names but it is– there is– you can be diagnosed 1.5. You have kind of a combination
of type 1 and type 2, they can see some antibodies in
your system, there may not be as much as in type 1 but they
can see some antibodies there that are starting to
attack your beta cells. And, but they may
not see a decrease of insulin for 5 to 10 years. So, sometimes they–
diagnosis type 2, but if they would take an
antibody test they would see that you are producing
antibodies. So, not quite type 1 because
you’re still producing insulin. And quite type 2 because
you’re producing antibodies, so it’s in-between,
it’s a type 1.5. So, there can be a
diagnosis of that. So, this in complications,
hypoglycemia, sometimes referred to as insulin shock because
of an increasing of insulin. So it could be– it could
be normal insulin production but you just didn’t eat right. I mean you didn’t eat breakfast
because you’re in a hurry, you had an emergency call
or something happened and you took your insulin. Well, the insulin is going to
work no matter if you ate food or not, this works, it takes
down carbohydrates and continues to work until it’s
done its thing. And so, it can reduce
your blood sugar levels and become hypoglycemic, or the
reason it’s called insulin shock because it’s the insulin
that’s bringing down. The other instance could be
that you take double injections. Now, you know, those of us who
don’t diabetes you’d wonder, well how in the heck could
someone take two shoots? Well it’s like anything else,
if you’ve done it for many, many years and it becomes a
habit then sometimes you forget if you did it. And I’m sure some of you
have gone through life and you’ve done things so
many times that every once in while you wonder, “Did
the turn the stove off? I can’t remember if I turn the
stove off,” kind of a thing. And– well insulin– diabetic
may get up in the morning, they’re kind of groggy
and they say, “I better take my
insulin before I eat,” so they take their
insulin and then, you know, they take their shower and
they do their thing and, “Jeez, I can’t remember — I
better take my insulin,” so they take another one. , you know, it’s just– [inaudible] wonder
why but it happens. So they get double insulin and it takes double
sugar, so that can happen. Hyperglycemia, ketoacidosis
again, [inaudible] often times
happen with individuals who have not in diagnosed yet. And so they don’t know
they have diabetes so they’re just munching
out like crazy. And so, they have an increased
food intake especially carbohydrates and their blood
sugar gets up to, you know, 500, 600, 700 and they just don’t
know, and so they go into coma, they can go into a coma. Both of these, you
can go to a coma. Or you can basically
forget to take your insulin. And you can– eat your food
and you’re in hurry and you, you know, you’re eating you
food and say, “Well after I eat, I’ll take my insulin,” and obviously you get an
emergency call or you just– you think maybe like,
“well, I already took it, I know I did, my insulin. So I know it, I don’t want
to take double so I’m going to just go like I did.” And so, like a 10:00 in the morning they start
getting the symptoms of hyperglycemia. And so we’ll talk about some
of the symptoms in that but, you can get shaky and– but obviously what
you would have is some of the symptoms we talked about earlier would be increase
urination, thirsty, hungry, you know, those kinds of things,
you know, would be a sign that you need to maybe
go see the doctor, you maybe hyperglycemic
kind of a thing. It doesn’t happen too
much in diabetics. You know, both these conditions,
most diabetics that are in diabetic for a while can
feel the symptoms coming on before it gets too bad
but if you misdiagnose, you’re undiagnosed and you
would know kind of a thing. So, what is your goal as
far nutritional therapy? So, here would be some numbers. Some of these won’t
make any sense yet but they will make
sense after we get done with cardiovascular disease. We talked about this preprandial
basically means before you eat. Postprandial means after
you eat, and usually, the blood test is taken about
two hours after you eat. And this is basically taken,
you know, just before you eat or after you wake up in the
morning or some thing like that. So, that’s what these
words mean. We’re going to talk this when
we get into the lipoprotein, so I believe it’s maybe
that even the next lesson. Well, I think we
did energy in that. But anyway, before
heart diseases, we’ll talk about these. But feel the LDOs are
considered the bad guys, HDLs are the good guys. Triglycerides, you
know what they are. So, these would be important
because if your member diabetics or 400 times or 400% higher
risk of heart disease. And so, these are
going to important for risk for heart disease. Blood pressure be important
because of, you know, high blood pressure
and your retinas and, you know, basically everywhere. And then sloughing
off of proteins that could signal
a kidney problem, so that’s in there the
BMI of less than 25. We’ll talk about BMIs. I think we’ll talk about
those later, but anyway. So, these are numbers
we’re shooting for. And these are numbers
that you’ll try as dry. That doesn’t mean you’re
ever going to meet those but these are our goals
that if a person just comes into your hospital,
they’re under your care, these would be goals
that you would tend to want to achieve, OK? When you get into working
hospitals, you know, hospitals are accredited. And so, they I think it’s
either three of five years, there will be team of
professionals that would come in and look at patients’
charts and look at things about the hospital and
reaccredit the hospital. Well, they will be looking
in patients’ charts, and so, they will know these numbers. But they really don’t expect
that for every single patient, you will reach certain number. That’s not their goal. The goal is going to be that
with the healthcare team, you are going to do
whatever it takes to try to achieve those numbers, which
means that everything needs to be documented in
the patient’s chart that you have done
everything possible to achieve these numbers. You have monitored
their blood pressure and you have counseled
them about blood pressure. You’ve maybe put them on
medication, you have talk to the patient, that’s where
the dietician comes in. They would talk to the
patient about their hemoglobin, about their glucose levels,
about their lipid levels and all of those, they would
talk to them and explain to them why it’s
important to get it down. The doc would possibly,
you know, prescribe Lipitor or something like that
to try to get them down. So, what the accreditation
team is looking for is have you tried to do it? They’re not really to
be honest expecting you to meet those goals because
everybody is different. You can expect everybody
to meet those goals. You cant’ expect perfection,
but the expectation would be that you have tried
to do everything. And the only thing that’s
going to be used as criteria as if you tried or not is what’s
document in the patient’s chart, basically, the premise is if it’s not written
down, it didn’t happen. So they can’t– If they
go on the patients’ chart, they see no documentation that a
dietitians talked to the patient about lipid levels or anything. Then, they’re doing to say– well, they’re going take
points off basically and that will do no good the
dietitians says, “Oh, yeah, I remember, I talked to
them on Tuesday about this and we discussed this. And you can talk to
the patient about it and they’ll tell you
we talked about it.” It holds no bearing. If it’s not written down,
it did not happen, period. So, these are the goals that
we’re trying to achieve. Hypoglycemia, let’s talk
a little bit about that because the nutrition care
plan for hypoglycemia, hypoglycemia are
basically the same. They’re both deal with
blood sugar levels and they’re both
dealing with a problem with maintaining
those glucose levels. So, they’re both
going to be dealing with how do we monitor
glucose levels. So, let’s talk about
hypoglycemia. And at the end, we’ll talk
about the nutrition care plan that would be for both of these. So, hypoglycemia is
below blood glucose. So, down to 45th, maybe the
normal is between 70 and 100. So, below 40-50, then
you would be diagnosed as being hypoglycemic. There– So, we talked about
epinephrine and the stress. So, if you’re under
24/7 stress back and cause your blood glucose
to go down, or worse would be if it’s a pancreatic tumor
that’s affecting the ability or sometimes it can cause the
increase production of insulin. And so, you’d have over
stimulation of insulin which it caused you
to hypoglycemic. So, hypoglycemia
is not a disease. It’s a manifestation of a
disease because if you remember, diabetes is a disease
because of hyperglycemia, because of ketoacidosis,
because of glycosuria. Hypoglycemia is a diagnosis. It’s a manifestation of
something else that’s occurring, so it’s a secondary issue. So, hypoglycemia is nothing– is something you should not
diagnose, self-diagnose. It needs to be diagnosed
by a physician where they do the
same exact things, glucose tolerance test fasting
glucose, the same things that you do with diabetes. And so, if you do
have hypoglycemia, they need to address
other issues and it’s not simply
a matter of, “Oh, let’s just give them
more sugar.” We’ll give them injections
of sugar to deal with their hypoglycemia because
that’s not the problem, OK? So please, if you have
friends that say, “Oh, I’m hypoglycemic,” and they
have not been diagnosed by a physician, you
should encourage them to go get diagnosed because
it could be something worse than they think it is, OK? OK, I’ll get off my soapbox now. But anyway, so there’s two
types, reactive is kind of the one that maybe
is more normal. And so, it would be more
common I guess, but basically after you’ve eaten a lot
of sugar, if you will, so go to a party cake and
icing like I saw in your mouth or drink punch, you’re whatever
in mono carbohydrates and that, you know, simple carbohydrates
and things like that, about two to four hours after
you eat it, you get the symptoms of hypoglycemia and I’ll go
over the symptoms in a minute. It could be because of an
over production of insulin. Insulin sometimes, if you hit
the system with a ton of sugar, the response of the pancreas
they’re producing could be over production because
it just kind of misdiagnosis how much
sugar is going to be there or it expects more
sugar, kind of a thing. So, the feedback is all these–
they’re eating pure sugar kind of a deal, and so
we need to prepare because if they keep eating
this, we’re going to need more and more insulin but you
don’t so you can stop. But so the over production of insulin can give you
those symptoms of that. It could be something else,
but sometimes it could be an over production of insulin. Fasting is more long term, it’s
going to be anywhere from 8 to 24 hours after you eat and you haven’t eaten
for a while, OK? So, it’d be something that maybe
you’d manifest when you wake in the morning after a
night sleep or something. But it could be an over
production of insulin but more of concern, it could
be a pancreatic tumor. So, this would be the
worse one kind of a things. So again, just don’t
self-diagnose. Here are some the symptoms,
again, shaking, sweating, dizziness, hunger, so these
would be the main ones. The top ones would be the main
ones that would be for reactive. So, you know, just feel kind of
goofy, you’re kind of sweating and you palms, your hands are
kind of sweating, you feel– the anxiety would
be not that your– I mean, you kind of feel
nervous but it’s kind of that like before an exam where
you have those butterflies in your stomach, kind
of a nervousness. So, it’s not a nervousness
or anxiety because of fear, it’s an anxiety of, you know, you just a little bit
nervousness, you know. OK, you know, again
like before an exam, it’s not like you’re
fearing, getting hurt or something like that. And then, you know, you
feel a little hungry but it’s not a painful hungry, it’s more of a sicky
butterfly hunger, you know, kind of a thing. Now, fasting is more the top and
the bottom, visually impaired, weakness, fatigue,
headache, irritable and those kinds of things. But just because somebody that’s
irritable dont diagnose them as being hypoglycemic, OK? But anyway, so these are
more severe type of things. So, if you know anybody that
goes through this and they say, “Oh yeah I’m a hypoglycemic,” so every time I get these
symptoms I just pop a life safer or I have some, you know,
glucose pills and dextrose pills or whatever and I just
pop them and I feel better if I ever think not
a good thing, OK? They need to go to the doctor. All right. So, what is a nutritional
care plan for both, you know, hypo and hyperglycemia
or diabetes? Carbohydrates should be still
about 40 to 50% of your diet. You should have or are going to do a meal plan using
carbohydrate counting. I put this in there
because I want you to know, it’s not that you would probably
ever do carbohydrate counting as a nurse or if you’re
going to be dealing hygienes or those something like that, but a dietician would
probably do that, but I think it’s
important for you to understand what
they’re doing. Because once again,
you are going to be the person
not the patient, is going to talk to most. Would probably do the
carbohydrate counting and all the stuff like that,
but the patient is going to ask you why they are putting
you on this plan that is going to be carbohydrate counting. So, I think it’s
important that you need to know how it’s
done just one done. And so, when you hear the word, you’ll kind of have
an understanding. And I think the only way to understand is
to actually do one. So, that’s why we’re doing it. It’s not to be mean,
it’s just hopefully to help you down the road. But basically, it’s
based on cards. It’s not based on
how fat much you eat, how much protein you eat, you
know, that kind of thing is because the carbohydrates are
going to turn into the sugars. So, it’s based on how many grams
of carbohydrates that you eat, and it’s based on
portions of 15 grams of carbohydrate servings
if you will. And they’re really called
carbohydrate choice, so you have 15 grams
choices that you can make. And so, the dietician will
go over carbohydrate counting with the patient basically
and usually the spouse if there is one or
significant other if especially they do the
cooking kind of a thing. And explain carbohydrate
counting and explain what it means and
basically it’ll take some time for patients to understand it. And but basically, it’s
just choosing foods that basically give
you a certain amount of carbohydrate choices, again,
15 gram choices per day spread out evenly through out the day so that you don’t have a big
push of sugar all at ones. So, when you do your carb
counting plan, what you need to understand is you may come up
with 20 choices of carbohydrates that you have to split that
and throughout the whole day. You need to make sure that you’re eating
basically six meals per day. And you need to spread those
20 carbohydrates over evenly as you can throughout
the six meals per day. So basically, you would have
a breakfast at 10 o’clock, snack at lunch, at 2 o’clock
snack, a 6 o’clock dinner and maybe an 8 o’clock
or 9 o’clock snack, OK. You cannot miss one
of those six. So, it’s basically 6
to 8 servings per day. You can’t really
escape one because– and an add to another
one because you’re going to have a big push of sugar
all at once if you eat a lot at one time, plus
your insulin level, especially your type
1 insulin levels and sugar intake are
going to be monitored. So, if you have like a
slower release insulin, you need to basically even out
your sugars throughout the day. Because if you don’t, then
the slower release is going to maybe release when you
don’t’ have very much sugar in your blood, you could
become hypoglycemic just for that instant. So, it needs to be spread out through the whole day
not skipping any of the meals and just even your
sugar all day. So, I think you’ll
understand better when you actually do the plan. It’s going to be difficult
for you to understand. But I think that puts you in
empathy with a diabetic patient who has not been to college,
who doesn’t understand, is not very good at math
and stuff how they feel. So I think it’s going
to put you an empathy with somebody who
has to do this. And so, I hope you
can appreciate why in having you do it even
though it will be difficult. So, don’t think that you’re
going to get it straight up, that you may have
to ask questions, but we will try to help through. And I think once
you’re through with it, I think it’ll help
you understand it but also understand what a
diabetic has to go through and I think that’s
important if especially if you’re not a diabetic. Glycemic index, we have a
little discussion about that. And so, you probably– I can’t
remember if you done it or not. But anyway, if you have– you understands the
glycemic index basically, it’s the premise of they took
white bread and they fed it to several people in the study,
and then after two hour period, they check their blood sugar
levels and they said, “OK, white bread will raise
blood sugar levels on an average this much
over in a two hour period.” And then, that was kind
of their base line. And then, they basically– they fix the scale of
all other foods based on a white bread being–
sometimes they use it the scale as white bread bring a hundred
and that’s the point scale for the glycemic or 70. It just depends on
which scale you use. But then, anything over that
number whether it’s 70 or 100, anything over that would be food that raise the blood sugar level
faster and higher in two hours. Anything below that would be
slower and lower in two hours. So, the goal would be to
choose low glycemic index foods that kind of either are low
in carbs or low in sugars or that the sugar
trickles in very slowly. And so, you might be surprised,
you know, because glucose– fructose has a lower
glycemic index than glucose because fructose takes
longer to be absorbed. We’ve seen that calories and
everything but if for diabetic, it can work better because,
well, it’s twice as sweet, so you use, you know, half as
much but also it trickles in. So, it has a lower
glycemic index. Glycemic load basically is if
you look at the glycemic index of some foods, they look high. But if you look at
the glycemic load which basically means how much
carbohydrate is actually there, even though the carbohydrate
that’s in the food would raise your
blood glucose very high, very fast, there’s
not very much there. So, the glycemic load
would be very low and I’ll show you
an example of that. So here is the idea is
that we have white bread and white rice are going
to be pretty much the same. But basically here,
the white bread, the glycemic index was 70,
so that’s that your goal. That’s the– Oh, and they’re
saying 59 to 60 as medium. Anyway, so I said there’s
different levels, but anyway, your goal would be obviously
in here in the medium range, so rather at 70 or so. So, you can see that white rice which would be some are the
white bread would be about in that range kind of a thing. But watermelon has a
high glycemic index. If we look around in back end,
I need more of that is bread or some kind I guess
would have higher. But you can see, bananas
even though they are fruit and seems sweet, they
would not [inaudible] because there’s a lot fructose
in there kind of a thing. So, you can see the
glycemic index but and then you would say, “Oh
based on the glycemic index, I wouldn’t– I shouldn’t
eat very much watermelon”. OK? Well, but if you look at the
glycemic load, there’s not a ton of sugar in watermelon. So therefore, it’s glycemic load or basically the
over all effect. It’s not going to be very high. So, you can see low as
10 and there’s a 3.6. So even though it has
high glycemic index, there’s not really much
carbohydrate there, so it’s not going to
be that big of a deal. Whereas you look
up here, you know, this has a high glycemic index
but also a high glycemic load so that would be kind
of a double-trouble kind of a deal here, so anyway. But white rice, not
a bad glycemic index but towards the higher and
they be of a glycemic load, so that’s the difference
between those. So, you know, this
is not something that you would send
a patient home with. This would be something that after the dietician
gets through, you know, doing a diet study
on the patient, basically doing a recall
or a diary or something on the patient, finding out what
they like to eat because, again, the premise is going
to be, you know, the patient may eat some
stuff they shouldn’t, but what’s the point? If you take away those foods
they enjoyed then are they going to really stay with it? I mean the compliance rate
in reality for persons on diabetes following a
diet is maybe about less than 20% to actually comply. So, if you give them something
that you know they’re not going to like, it ain’t going to work. It’s just, it be lower than 20%. Anyway, so you work with
the patient, you allow them to have some foods they enjoy
but try to limit them especially if they’re high glycemic index,
high glycemic load foods, you would basically say, “OK. These are very– These are going to raise your blood sugar
really fast and a lot.” So, what we need to
do is I’m not going to completely take them
away from you but we need to really cut down
on your portions of how much you eat
per week or per day. And so, if they like to eat
something high, you know, everyday, then you would
possibly say, “Well, could we try maybe– maybe you
could try just eating them– eating it four times a weeks.” You know, the same
amounts that you normal eat but four times a week
instead of seven. Could we try that,
kind of a thing? You think that would
work kind of a deal? If they say, “No”, then
you would say, “Well, would it be possible that
we could try maybe half of a serving per day for seven
days a week instead your whole servicing, instead of
eating a whole cup? Would you be willing
maybe to try a half of per cup a day
kind of a thing?” Anyway, you can get it, but
the idea would be to try and decrease those glycemic
index, glycemic load foods as much as you can
because, you know, they’re going to be the problem. So anyway, but, so you
wouldn’t send home the patient and with a big book because
there’s a big book and this and say, “Well, you need
to look up every food and see what their glycemic
index is, a glycemic load and we need to, have
you document this? And then you going to
follow these completely.” That’s not going to work. So, you just kind of use
this as a tool to help them to make better choices. Oops. Let me do something here
for some reason is not going, so I want to continue recording. But we’re missing some steps. So, let me go here. And how am I going to
do this slideshows? There we go, set slideshow. I need to go up two
more pink, pink. 64. OK. So now, we can go. So, we’re going to
go here and here. Sorry about that. So now, you know, how I set
my PowerPoints but anyway. So, we talked about the glycemic
index and that of things. So, the next point would
be how much protein? Well, 15%, that’s a higher
then what we talked about, we talked about 12%. And so, but we’re deemed
with our immune system here, we need to make sure we
get plenty of protein that can be dealt with the
immune because we’re going to be a little compromises
there, we need to keep up their immune system
in that kind of thing. But it needs to be
[inaudible] foods, things that don’t add a lot
of fat and that kind of thing, lipids, 30% of your
diet or less if you can. And then, you know, again, these
are all going to be related to heart disease, so we need
to make sure we monitor those and how much that
we get of those. But pretty normal that
way, multiple feeding as I mentioned, 68
feedings per day. Trying to even out especially
with the carbohydrates, trying to even out the
amount of sugar that goes in the blood system one time because you have a compromised
blood management system if you will. And so, you need to
just trickle things in, even it out throughout the day. And then, kind of balance
that reasonable way, again, below BMI of 25, if you can
but sometimes difficult. But if you can do it, then great because that would mean the
patient doesn’t have to go on insulin, doesn’t get
pancreatic exhaustion that kind of thing. Alcohol, limit to
one drink per day and one drink is considered 12
ounce of beer, 5 ounce of wine, 1 1/2 half ounces of liquor, OK? If you can, I mean, again,
the alcohol is going to mess with your cells, all right? And so, the more– if you
can get the person not to drink alcohol, the better. But is that realistic? Probably not, especially if they out to dinner and
they enjoy wine. But try to encourage
them to limit it to one drink a day
if they can, OK? But that will be up to them. You know, you can only make a
patient do what they want to do. If they don’t want to,
they’re not going to but you can encourage
them to do that. So, that’s carbohydrates. I know it’s kind of a
long drawing out lessen, but you’re going to
encounter a lot of diabetics. I wanted you to know as much as
you possibly can about diabetes. And hopefully, this would
kind of stick with you. And when you get to be a
healthcare professional, if somebody has diabetes,
you can either to go back to this stuff or you can– at
least, you can remember some of it and encourage them
but also and be able to answer their questions,
all right? So it we’ll–
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