The Dr. Hyman Show - Exclusive Dr. Hyman+ Functional Medicine Deep Dive: Polycystic Ovarian Syndrome (PCOS)
Episode Date: January 2, 2024Hey podcast community, Dr. Mark here. My team and I are so excited to offer you a 7 Day Free trial of the Dr. Hyman+ subscription for Apple Podcast. For 7 days, you get access to all this and more ent...irely for free! It's so easy to sign up. Just go click the Try Free button on the Doctor’s Farmacy Podcast page in Apple Podcast. In this teaser episode, you’ll hear a preview of our latest Dr. Hyman+ Functional Medicine Deep Dive on polycystic ovarian syndrome (PCOS) with Dr. Carrie Jones. Want to hear the full episode? Subscribe now. With your 7 day free trial to Apple Podcast, you’ll gain access to audio versions of: - Ad-Free Doctor’s Farmacy Podcast episodes - Exclusive monthly Functional Medicine Deep Dives - Monthly Ask Mark Anything Episodes - Bonus audio content exclusive to Dr. Hyman+ Trying to decide if the Dr. Hyman+ subscription for Apple Podcast is right for you? Email my team at plus@drhyman.com with any questions you have.  Please note, Dr. Hyman+ subscription for Apple Podcast only includes Dr. Hyman+ in audio content.
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Hello, my name is Dr. Keri Jones and today we're going to talk about polycystic ovary syndrome. This is a functional medicine deep dive for the Dr. Mark Hyman Community Plus,
and I am really excited to go over PCOS with you today. I've got a lot of information to cover
because I think PCOS really gets misunderstood, and it's just so common that it is important
you understand this so you can feel empowered when you're talking to your practitioner about what's going on,
or if maybe you suspect you have PCOS or you're confused about PCOS, then listen along as we jump in.
We are going to cover the facts about PCOS, signs and symptoms, the Rotterdam criteria,
hormone pulses really essentially is how hormones work in the body, insulin, inflammation, and
visceral obesity, which are not part of the Rotterdam criteria but are still important,
the PCOS evaluation, conventional PCOS treatment we will touch on, and of course a more functional
approach to PCOS. So a few caveats before we get started, of course. This is going to be about a 90-minute webinar. It will focus a little more, or I should say maybe a lot more, on insulin and inflammation.
Because please keep in mind, even though none of those are part of the Rotterdam criteria, you can be any age, really. You can be any size. you can be any ethnicity, it doesn't matter. Insulin and inflammation play a big role in PCOS.
And so I want to make sure that you are empowered in understanding this information and not
blown off or gaslight or told it's not possible for you when PCOS might really be possible.
I'm going to introduce some interesting research that maybe the average practitioner doesn't
know.
And maybe I have actually had patients who've said, you know, I actually brought this up to
my primary care or my OBGYN. And they were like, no, that's not true. And in fact,
it's literature from 2000, 2022, 2023, and they just maybe hadn't read it yet. It hadn't come
across their desk. And so by knowing this information, again, you're more empowered to seek the help that you need and make changes. So I'm not going to focus on like the
conventional therapy, such as the birth control pill. I will touch on a number of conventional
therapies so that you know what is out there. They may be the right decision for you. I'm actually
going to talk more about the functional medicine options for PCOS, just because I think you're probably in
Community Plus or watching this webinar because you've been offered a lot of the conventional
therapies and either you had side effects, they didn't work for you, you're maybe trying to avoid
them for certain reasons, or maybe you'd like a combination. Some of the conventional therapies
work great for you and you are still struggling and looking for other options for other signs and
symptoms that you're having. Please know it is okay to get a second opinion. If you listen to
this and you think, I knew it, I knew I had PCOS, or I think I really have PCOS, it's okay to seek
out somebody else who will listen to you. And it's also okay to have multiple practitioners
on your healthcare team. So if you really like your OBGYN for basic OBGYN
type of care, your annual physical and PAP, but you don't feel your OBGYN is listening to you
regarding these symptoms, please feel free to seek out somebody else who maybe is a lot more
experienced with PCOS, educated. Maybe that's the only thing that they focus on
in their practice. And it's okay to bring
those two together and get the help that you need. Okay. So before we get into the juicy stuff,
like signs and symptoms or treatment and lab workup, I got to give you some quick PCOS facts.
So here is a biggie. PCOS is the number one endocrine disorder in females. The number one. However, it's thought
as many as 75% of patients with PCOS are unidentified in clinical practice. And this
drives me absolutely nuts. We know it's the number one endocrine disorder in females, and yet as many
as 75% are still unidentified or gaslit or blown off, or maybe it's not considered important to
work up for a while. I've had people tell me it took them years, five years, 10 years, 15 years.
I've had women in perimenopause say, you know what? I had all these symptoms. Nobody took me
seriously. And finally in perimenopause, I switched doctors and was told I probably had PCOS that
whole time, that whole time. So listen along, take notes. And
if you definitely feel like you're raising your hand, nodding your head as you're going along,
don't be part of that 75%. Don't get blown off because there is a lot that you can do.
It is a major reason, PCOS is a major reason for oligomenorrhea and fertility challenges. Oligomenorrhea is just a fancy word for
generally long irregular periods. And I'll have a slide on this in a little bit. It's longer than
35 days. So if you find you have irregular periods or they're really long, you're skipping months,
they're 40 days, 60 days, 90 days before you get a bleed. Sometimes maybe you've go six months
without a bleed and you should be bleeding and you should be bleeding. This isn't somebody maybe who's 51,
52, where you expect they're, you know, really headed into menopause and they're going to have
irregular cycles. I'm talking, maybe you're listening to this in your teens, twenties,
thirties, and you're like, wait a minute, this is me. And this, these symptoms have been here
for a while. Additionally, PCOS is probably a number one thing that should be worked up if you are
struggling with fertility and nobody is bothered to look into some of the markers we're going
to talk about.
I really want you to know that it's the major reason.
It's the major reason for long irregular cycles and fertility challenges.
And when it comes to the cause, the reason, the why behind PCOS,
it's a conglomeration of things. So it's genetic. I'm going to point out some genetic snips.
It's environmental, wreaking havoc on those genetic snips, lifestyle factors,
wreaking havoc on those genetic snips and how it all comes together. So there's not really
one thing. I know a lot of us would like to find the one thing,
the one single root cause that we can go after and address for PCOS, but that's not how it works.
It is a multifaceted endocrine system that requires a multifaceted approach. With PCOS,
it's not just about your cycle or fertility, if that's of interest to you.
The long-term sequelae, so the long-term consequences, if unaddressed, are a much higher risk for cardiovascular disease, type 2 diabetes.
If you are listening to this or you've already been diagnosed withHEA, which are all hormones we'll talk about, and the symptoms to go with it. And nobody has talked to you about cardiovascular
disease, getting advanced cholesterol testing, lipid testing, blood sugar and insulin testing.
You probably should bring this up with your practitioner because the long-term consequences
are higher for you to go on to develop these. We know cardiovascular disease is the number one
killer of humans. Why be at higher risk factor? Make sure that you're getting this evaluated.
Bring this up to your practitioner of, hey, I have PCOS. You've diagnosed me with PCOS.
Let's really tackle the cardiovascular aspect,
or sometimes we call it the cardiometabolic aspect because of that diabetes insulin risk.
And lastly, how do you diagnose PCOS? Well, there's a few different ways, but the most common,
the most, I would say, widely accepted is the Rotterdam criteria. So what is the Rotterdam
criteria? Why have we all kind of settled on that? Before we can get into the Rotterdam criteria? Why have we all kind of settled on that?
Before we can get into the Rotterdam criteria, what does PCOS look like?
So as you're looking down this, do you check off any boxes, irregular or absent menstrual cycles?
But yet you should have a menstrual cycle.
Hirsutism.
So dark hair growth on the chin, down the neck, around the nipple, or the umbilicus.
And I don't mean like the one annoying chin hair. We all have annoying hairs that grow. Hairsuitism is more significant. I'm
going to show you a chart as we get into the workup part of where on the body we look for hair.
This can also be separate for an ethnicity that tends to grow a lot of dark hair in these places,
on the chin, down the neck, around the nipple, the umbilicus, et cetera. So it is something that you have to pay attention to and to be aware of if you have
a family history of your moms, your aunts, your grandma, your sister, they've all grown dark hair,
but PCOS is not the issue. Probably looking at more of ethnicity as opposed to driven by these
androgens. If you have the one annoying chin hair,
two annoying chin hairs, that's not what I'm talking about either. Acne, particularly cystic
acne here on the chin and the jawline. Obviously you can get acne all over the back, the chest,
the neck, the forehead, your cheeks, all over the place. But particularly this type of acne,
we're thinking chin and jawline. Hair loss at the crown or the
temples. So sometimes depending on the location, we will call it a female or male pattern baldness
just because of the location of where it tends to show up. That central visceral adiposity,
so the visceral fat that's around your organs. Skin tags. And again, I don't mean like one skin
tag. If you're like, oh gosh, I have a skin tag
in my elbow crease. The one skin tag is what I'm talking about. But if you notice you're developing
more skin tags, especially like in your neck or in your armpit, then we got to talk. Acanthosis
nigrans. This is that darker, thicker skin that tends to be in the folds of like your armpits,
the nape of your neck, just sort of
anywhere really that you've kind of got folds. Usually it's on the upper body and you can't
wash it off. You may scrub it with a washcloth and you find that it's not coming off. It's known
as acanthrosis nigrans. And if you haven't seen it, I strongly suspect looking up online for a
picture to see if this sounds like you. And this isn't just dirt. This is
a byproduct of these hormone changes in PCOS. Metabolic dysfunction. If you already know you
have glucose insulin issues, if you already know that your lipids, your cholesterol are higher than
they should be, if you already know inflammatory markers are higher, you've got a lot of inflammation,
it can go along with PCOS. And of course, fertility changes. So you've been
struggling to get pregnant. Maybe you don't ovulate because you have really long irregular
cycles. You're considering fertility workup. And you check off some of these other boxes.
Make sure you have been evaluated for PCOS. So now that you know these are sort of common
symptoms of PCOS, you do not have to have all of them by any stretch. But you also may notice some of these symptoms, like I said,
the one chin hair, the random skin tag. That's not what we're talking about for PCOS. PCOS is
a syndrome, right? It's a multitude of things in quantity that comes together. So now let's move
on to the Rotterdam criteria now that you know those symptoms, when you have the diagnosis of PCOS, you need to have two out of these three
to be considered PCOS. So not one, and you don't have to have all three. You have to have two out
of three. So first and foremost, do you have irregular cycles longer than 35 days or complete
absence of cycles? If you said yes, you've got number one. Number two,
hyperandrogenism, high levels of androgenic labs like testosterone and those androgenic symptoms,
hair loss. I'm not talking like the golden retriever type of hair loss where you just
sort of shed all over. It's usually crown of the head, temples, androgenic alopecia,
maybe you've been told that. And then of course, the cystic acne on the jaw, the chin, the hair growth in places you don't want it, the hirsutism, but generally
significant. Again, not like the stray hair, not like a little bit of lip hair, upper lip hair.
With hirsutism, it's more significant than that. And third, polycystic ovaries. We call it
polycystic ovarian morphology, PCOM. So polycystic ovaries. We call it polycystic ovarian morphology, PCOM.
So polycystic ovaries and ultrasound.
Despite the fact that it's called polycystic ovary syndrome, you don't actually have to
have polycystic ovaries and ultrasound.
You can have number one and number two, and that's considered two out of three.
But you can also have polycystic ovaries and irregular cycles and not have hyperandrogenism
and still be considered PCOS. And you can have
any combination thereof, which means PCOS can be tricky to diagnose and also why some practitioners
maybe have blown you off. Maybe they'll say, you know, we did an ultrasound. You don't have
polycystic ovaries, so it's not possible. It's totally possible. You don't have to have number
three, but if you have number one and number two, you qualify for the Rotterdam
criteria. So let's hone in on that polycystic ovaries because of polycystic ovaries, the
qualification as of late is that you have to have 12 or more follicles measuring two to nine
millimeters in diameter or increased ovarian volume.
This means sometimes they call it like a string of pearls. You can see follicles are the like cells around the egg that would normally hopefully ovulate. And they're in various stages of growth
and maturity before you actually get to the month where it's going to ovulate. And so when you have
so many, 12 or more, that are
kind of around a similar size and not progressing, and it looks like this, all the little numbers on
here are follicles, that's when we definitely think, oh my gosh, this poor ovary, it is just
swarming in follicles and they're not really progressing. They're not getting bigger and
they're not getting smaller. This is likely in that polycystic category, that number three.
Here's the caveat.
Do all ovarian cysts mean PCOS?
I've absolutely had patients who've said to me, I have PCOS because on an ultrasound,
I had one cyst.
I had one cyst.
And it's just simply not true.
You have to fit that polycystic ovarian morphology.
Now, can you have number one, number two, so irregular
cycles or absent cycles, hyperandrogenism, and happen to have a cyst on your ovary? Of course
you can. Of course you can. But it's the multiple cysts, 12 or more, that are two to nine millimeters
in diameter on a particular ovary or on both ovaries., if you've gotten an ultrasound before and they've told you,
you have one single cyst, that's not the definition of qualification to fit in the
Rotterdam criteria. You still have a cyst. I'm not denying that, but a polycystic, poly means many,
right? So you have to have many, 12 or more. When it comes to this, as I said, you can kind of have a variety of types. So there are four
phenotypes of PCOS. Phenotype A is the most common. 44 to 65% of women have it. You tend to have
polycystic ovaries. You have all three. You have oligo and ovulation, which basically is a fancy
word for irregular, and you don't ovulate. You don't release an egg. And then all the
hyperandrogenism, all that testosterone, all the symptoms that go with it.
That is the most common.
The second most common, but not by much, is where you're not polycystic.
You don't have cysts in your ovaries, but you still have the oligoanovulation and the hyperandrogenism.
So you go in for an ultrasound and they say, nope, your ovaries don't have any cysts in them.
They're not polycystic, but you have everything else.
C is when you are polycystic, but you still get your period every month. It's normal. It's consistent. It're not polycystic, but you have everything else. C is when you are polycystic,
but you still get your period every month. It's normal. It's consistent. It's not absent. It's
not all over the place, but you also have all of the androgen symptoms. You have acne, you have
hair growth in places you don't want and hair loss on your head. And so B and C percentages are really
pretty similar. And so, and then finally we get to D, which is where you're polycystic,
your cycles are kind of crazy, but you don't have any of the androgenic symptoms. You don't have acne, you don't have hair growth in places you don't want, you're not losing hair more than
the average bear. And now right where that zero to 23%. And so you can see D, C, and B are why
it can be frustrating for a lot of people trying to understand if they have PCOS. A is the most
common. It doesn't mean it's the only phenotype out there. And by understanding this, you can go
to your practitioner and say, hey, look, I think I'd like to get an ultrasound first and foremost,
because I fall into the menses or the androgen category as an example. And so if they come back
to you and say, no, no, that's not possible. You don't have cysts on your ovaries. You can go, that's fine. I might be phenotype B. 8 to 33% of people with PCOS are phenotype B. I'm trying to figure out if that's me. um, easy classical way to diagnose. There is what we call more like a classical look
or a classical symptoms with PCOS, but there are four phenotypes, which means the lesser known or
the lesser common phenotypes just aren't given as much attention. And by you understanding this,
now, you know, you can get the help that you need. So when I mentioned earlier that why PCOS develops is kind of a, it's a syndrome.
That way that means that there's a lot of parts involved. So they say the proposed
pathophysiology of PCOS is a synergistic relationship between perturbed gonadotropin
releasing hormones, GnRH, pulsatility, hyperandrogenism, probably accompanied by hyperinsulin, insulin resistance,
and inflammation. All right, hold on. Huge words, crazy. Let's break this down so you understand
what's going on with PCOS. So first of all, pathophysiology is just basically like what's
happening in the body, right? What's the pathology and physiology in the body? What's going on with
my anatomy, my biochemistry, and everything that creates all this PCOS. Perturbed GnRH pulsatility. So GnRH is a hormone, a master hormone that comes
out of your brain and it pulses. It pulses. Hormones, all of them are pulsed out. They are
not continuous like a hose. It's not like one day your body says,
you know what, you need progesterone today and just turns on the hose or turns on like the
kitchen sink. It doesn't do that. It pulses it out like Morse code. If GMRH needs your ovary
to make progesterone, it's a very specific Morse code it gives out. If G on RH needs you to make testosterone,
it's a very specific Morse code that comes out.
There is no switch flipped on.
It does not look like this picture
where the pulse or the hose is just on continuously.
So don't think this.
Don't think it's a continuous hose at all.
We wanna think of it as a pulse.
So think about your heartbeat, right?
Your heartbeat, while your heartbeat is a continual beat, there is a rest in between there. It's a pulse,
not one just straight line that's high all the time, right? We get a heartbeat,
slight rest, heart rate, slight rest, heartbeat, slight rest. Your hormones are similar depending
on what they're making. Estrogens, progesterone, testosterone, et cetera.
So pulsed out, remember pulsed out.
So with that GnRH, your brain and the part of your brain called the hypothalamus pulses
out GnRH.
This goes to a different part of your brain called the pituitary.
Depending on what the Morse code is from GnRH, you're going to make LH or FSH.
You maybe have had these run before as part of your menstrual cycle.
LH is luteinizing hormone.
FSH is follicle stimulating hormone.
They rise and fall at different parts of your menstrual cycle to help you ovulate or to
make estrogen or to stimulate progesterone or stimulate testosterone.
They do work on the hormones.
Then the brain goes down to your
ovaries because LH and FSH have their own Morse code. They have their own pulses. So everybody's
pulsing. Everyone's Morse coding to each other, depending on what you need. So FSH stimulates
follicles to grow and stimulates estradiol to be made. LH stimulates androgens like testosterone,
ovulation, so you release the egg, and then
progesterone once you release the egg. So you can see Morse code essentially is a big part of your
body system in making all of this happen. So as I said on that first slide, that was really
confusing, GnRH pulsatility. So somewhere, some reason around these lines, your Morse code's getting messed up.
It's either getting blocked or it's getting diverted.
It's getting changed to some other code.
So the rolling thing is getting pulsed out or they're not listening.
Somebody is not listening to the Morse code when it comes to this.
So what affects these pulses?
Pretty much everything. Everything from like chemicals to stress to illness,
if you've been sick, to changing time zones, to medications.
So many things affect the pulsatility.
But in the case of PCOS,
as that really confusing slide said earlier,
insulin, hyperinsulinemia, insulin resistance,
and inflammation, absolutely.
So insulin and inflammation. So we have to talk about this when it comes to PCOS. Before we get there though,
you might be into genetic SNP testing. Maybe you've had some sort of testing done because
you're curious about something like your COMT or your MTHFR. But there are specific SNPs. In fact, I was reading a research article that
said there's 30 plus SNPs being studied, and this is just a handful of them, in PCOS. There is some
sort of variant in those with PCOS causing all sorts of issues and symptoms. Here's the kicker.
30 plus SNPs are being studied for PCOS, which means this is why
it can maybe hard for you to get diagnosed with PCOS because of a 30 plus SNPs, you may only have
one or two variants in some of these where somebody else may have 20 plus variants in these.
And so your symptoms may not exactly look the same. Your workup may look a little bit different.
Your practitioner may struggle to try to get you diagnosed because it's not cookie cutter. Nobody, none of this is cookie
cutter. There's similarities and overlap, but please remember it's not cookie cutter. So you
can see in this, just this short little list, if you're, if you're familiar with SNP testing,
insulin receptor, well, that's super important, right? Things that have to do with how you make or don't make fat tissue.
Adipogenesis.
Adiponectin.
CYP1A1 has to do with how you detoxify a lot of things, but particularly your estrogens.
Your risk for type 2 diabetes, cardiovascular disease.
So type 2 DM at the very bottom is diabetes, mellitus.
And then CVD is cardiovascular disease.
So if you have a variant in your PON1, you're at risk for a few things, but you're at risk
for type 2 diabetes and cardiovascular disease.
If you have PCOS, you're at higher risk for this anyway.
And so now you throw this on top of it and it's bad news bears.
FSH receptor.
So now you're trying to get FSH to bind a receptor
so it does its thing, makes estrogen, grows a follicle, has a healthy cycle, and if you have a
variant, it may not be able to communicate. It may not be able to hear the Morse code effectively.
The androgen receptor. I would imagine if you've been struggling with androgenic symptoms,
hair growth in places you don't want, cystic acne, hair loss on your
head, is it possible you have been trying treatments and they're not working? And or
maybe you've been doing blood work and you've been told your androgens are in range.
Your testosterone's fine. It's totally where it should be. Your DHEAS is fine. It's totally where
it should be. It's possible. We can't test
this yet. We just know the SNP variant's there. It's possible the receptor, let's say cystic acne
in your chin. You have a lot of androgen receptors here. You just do. And it's possible your receptor is more reactive. It gets triggered faster when testosterone comes by.
If I have a testosterone hormone float by my androgen receptor in my chin, I'm not going to
react. My receptor doesn't care. My testosterone doesn't activate it. I don't get cystic acne.
You have an androgen receptor variant. You have PCOS in this example.
You have a testosterone float by. Your receptor freaks out, gets dramatic, turns into a diva,
pops out of cystic acne. The heck? What? So you may have normal levels of androgens,
but all the symptoms because you have a variant in the receptor. It's not fair.
I don't know who designed it. I would like a word with them, but it is something that they're
studying. So even in lab testing, it can be frustrating because you've been told, quote,
unquote, everything looks normal and you truly may fall in the range, but the receptor is super
sensitive, super dramatic, and it's going to react dramatically anyhow, no matter what.
It's not fair.
Antimullarian hormone, AMH.
This is a hormone made by your follicles.
We'll talk about it when we get into treatment.
So you can, TNF-alpha, IL-6, these are inflammatory, inflammatory, increased inflammation.
The variant in these, you're more prone to getting inflammation, et cetera. So you can see right away, I'm really happy that the genetics is moving in this direction
with PCOS because it doesn't mean you've lost all hope.
Just because you have a genetic issue, you've got some sort of variant in this, does not
mean there is nothing you can do.
There is so much you can do, and that's how we're going to talk about it.
But I do need you to understand that they're still testing this. They're still researching this. They're still looking at this.
Like there's a lot for PCOS and there's a lot they're still uncovering. So if you have genetic
variants, if you've been doing any kind of genetic variant testing somewhere and you get told, you
find out, you read the report, you have some of these variants and you're thinking, oh my gosh,
I was born with this. What do I do? Your best. Okay. You're going to do your best with what you know. And that's why
you're here watching this webinar, because I'm going to arm you with a whole lot of hope and a
whole lot of information about your inflammation, your insulin and lifestyle and PCOS and all the
things. So hang on, here we go. We are first going to look at high insulin. I know
not everybody has high insulin with PCOS. However, it is ridiculously common and it's more common
than you think because I feel, and a lot of functional doctors feel, that the insulin range
is wrong. And I'm going to show you the studies to back it up. Having high insulin is not a criteria
for PCOS in the United States. I have
read in the literature in Asia, certain countries in Asia, they do take the metabolic aspect into
account with PCOS. We may get there someday. Rotterdam criteria gets debated all the time
as the criteria that we use because high insulin really is so common. But here's the thing about insulin that I need
you to know. There's four major PCOS effects. There are more than this, but these are the major.
So again, pulsatility, pulse, not hose, Morse code, right? With high insulin, you get an
increased GnRH pulse. Now your Morse code speeds up. When it speeds up, you're going to have higher
LH luteinizing hormone. Luteinizing hormone is the Morse code for you to make androgens. So now you have more of those.
And when you have higher androgens, you may not ovulate. So you're not going to release that egg.
So when you don't ovulate, you're more prone to getting cystic ovaries. Now you have high insulin
creating all that androgen production directly from the ovarian cells. When you have a lot of LH, then the follicles themselves can make
the cells in there called theca cells with a TH, theca cell, they make androgens. They make
like in the cell itself, and then they let about 20 to 25% of it go out in circulation.
So they pump that up inside the follicles. In the bottom left corner, high insulin
decreases something called sex hormone binding globulin, SHBG. It was too long to write it out,
so I had to shorten it up. SHBG. You've probably heard of SHBG before. It's commonly run with
testosterone. It's talked a lot about males and not enough in females. We have it too.
And what SHBG does, it's a bus, hence the emoji.
It is a bus that binds up testosterone or like a sponge that mops it up. So if you have low levels
of SHBG, low buses, then you have a lot of free testosterone. They're all standing around the bus
corner like, where is the bus? I need to get on the bus. And when you have a lot of free
testosterone, free hormone, if it has the word free in front of it, then it's free and active and able to bind to receptors, activate the receptors, and do the thing.
Now, we like testosterone, right?
We like it for our joints.
We like it for our bones.
We like it for our brain, our mood, our libido.
But too much, and now we have hair loss, cystic acne, and hair growth in places we don't want.
We have the skin tags.
We have acanthosis nigrans. It all contributes to all of that. So it's kind of Goldilocks-ish. Too much
is a problem. Too little is a problem. We want it to be just right. So when you have high insulin,
you lose out on those buses. So now you have all this excess free testosterone that's being created
to bind to all the places we don't want and cause problems. And lastly, the fourth big thing is
increased insulin favors the development of that visceral adiposity, the visceral adiposity, which is
around our organs, which is the worst kind. Adipose tissue makes its own inflammatory markers.
It's very inflammatory on its own as tissue, that visceral adiposity. And remember, I say this later, you can have, you can be what we,
you know, what's commonly called skinny fat. So you can have a lot of that unhealthy visceral
fat tissue around your organs and be what's considered a normal like height and weight
for your age. You can have, you can be a higher, right? Higher weight for your age and for your age. You can be higher, right? Higher weight for your age and for your height. You can
be underweight and still have, again, that skinny fat. You can have a lot of that visceral adiposity
around your liver, around your heart, around your pancreas, et cetera. So please don't mistake when
I say visceral adiposity that I am always talking about somebody who is overweight or obese. You could absolutely be
listening to this, thinking to yourself, for my height and my age, I am the perfect weight.
But inside, you have a lot of adipose tissue. When you have all that adipose tissue, it creates a lot
of inflammation, like fires. It also can increase estrogens, particularly one called E2, which is
estradiol. So your adipose tissue can take testosterone and convert it into something
called androsenedione, which will then convert it into estrone, convert it into estradiol. So
basically it's this whole cascade for you to make excess estrogens right there in your fat tissue.
So now you have increased inflammation, increased estrogens, there in your fat tissue. So now you have increased inflammation, increased
estrogens, increased cardiovascular problems. So the four areas that insulin can really screw you
up. When we get into the nerdy side of it, you can see right in the center, insulin resistance,
chronic inflammation, and then we get into showing, again, hyperinsulinemia. So high insulin
affects the pulses. We have high androgens. We have the polycystic ovarian
morphology. And at the top, we have like other contributing factors, other hormones
that can worsen the issue. And even in the literature, even in the research, this is 2014,
so nine years ago at the time of this, showing how the spider web is all connected and why we
need to address all this. So increased insulin and increased insulin resistance is extremely
common in PCOS. It is not a Rotterdam criteria, but it is something you don't want to miss.
And both obese and non-obese PCOS can have insulin problems. So if you, again, if you are listening to this and you're thinking,
can't be me, I am the acceptable weight. I think I'm a healthy weight for my height and my age.
Can't be. Always check your insulin anyhow, especially if you're like, weird though,
because I have cystic acne and I have hair loss and I'm having all these other symptoms. I have
irregular cycles and I'm struggling to become pregnant. Get your insulin checked at the very least. So let's talk about
insulin. I mentioned, I don't like the reference range for insulin. So when we look at insulin,
insulin is not commonly done. Oftentimes your doctor will do a glucose, a fasting glucose,
or they'll do a hemoglobin A1C, which is a kind of a sort of a summation of glucose over time, but they never
run insulin. And it's so frustrating. You want to ask for a fasting glucose and a fasting insulin
together. So I have circled here. What is the range? Conventional labs, your typical laboratory,
typical hospital says anything under 25 is considered normal. You can be 20, 21, 22, 23, 24, 24.9, and you will be
considered having a normal insulin. Not quite the case. We want our fasting insulin to be
lower than that. A study done in 2018 evaluated fasting insulin called FI and the risk of
metabolic syndrome. What is metabolic syndrome? Metabolic syndrome is obesity, high blood pressure, high blood triglycerides, when you get that cholesterol
panel, low levels of HDL cholesterol, and insulin resistance. When you develop metabolic syndrome,
of course, your risk for all things cardiovascular disease goes through the roof, and we are trying
to prevent that. Cardiovascular disease is the number one killer of humans. Let's prevent the risks. So back to our study, 2018, they said, all right,
fasting insulin, what level increases the risk of metabolic syndrome? So this is what they said.
After adjusting for gender, age, BMI, smoking status, hypertension, and dyslipidemia, so
high cholesterol stuff, middle age and elderly
population in the high fasting insulin group were at a significant risk for developing metabolic
syndrome so I read this part and I'm thinking cool right anything over 25 right because 25 is the
normal cutoff for labs and hospitals and whatnot high fast insulin group significant risk for
developing metabolic syndrome this conclusion is consistent with previous findings.
So other studies have figured this out prior to this 2018 study.
Cool, got it.
What is considered high fasting insulin?
They said high fasting insulin out of 104 people was anything greater than 7.9.
7.9.
Not 25.
7.9. Not 25. 7.9. They considered a moderate fasting insulin level to be between 4.9 and 7.8.
Not 25. 4.9 to 7.8. So when you talk to somebody who's maybe more functional,
integrative, holistic, naturopathic, they'll probably tell you that they want their insulin in their ranges to be a lot lower than 25. Commonly, although this is not
set in stone, commonly you will hear things like, I want it under seven. I want it somewhere between
two and five. This is why. they're trying to mitigate you having metabolic
syndrome and increasing your risk for cardiometabolic disease down the road. So if you
have an insulin, a fasting insulin in your blood work recently in the past, somewhere in your
records, pull it, go pull it and look and see where it's at. Are you two to five? Because remember two to
five is to get below what's considered a moderate fasting insulin. This is fasting. This is no food,
right? I'm not talking about your food response, your insulin response to food. I am talking about
you wake up in the morning fasting, go to the lab, get your blood drawn. What is your insulin?
It should be nice and low. You have no food in your system. It should be nice and low. So this is why you will often hear people in, again, that functional
integrative holistic community say, we want your insulin to be well below 25. We are trying to
prevent you from developing metabolic syndrome and further cardiovascular disease. You can show
your practitioner the study if they disagree. If your practitioner tells you that you have a 19, a 20, a 21, a 15, you're fine.
I have unfortunately even had practitioners tell patients that even in the mid-20s is fine.
Really, once you get up into the high range, the 40 and 50 range, that's when we get concerned.
I was like, good gracious, that is not when we get concerned.
We get concerned a lot sooner than that. That's why we call this a more functional,
holistic, integrative approach, right? This is the functional medicine deep dive for a reason.
Okay. Now that you are fully versed on insulin, you're going to go request insulin. You're going
to pull your lab work on insulin and see what your last insulin was. Hopefully it's somewhere
in the two to five range. Let's talk about inflammation and PCOS.
Inflammation basically is finding and fighting fires. What is inflammation? Fires. Many fires,
moderate fires, big fires. Reports show that women with PCOS, both with obesity and normal weight,
exhibit elevated serum TNF tumor necrosis factors, C-reactive protein, monocyte lymphocyte
circulating levels,
and inflammatory infiltration in ovarian tissue. What does this mean? TNF, C-reactive protein,
monocyte, lymphocyte circulating levels, again, all fires. There's inflammation happening.
And so everybody, the alarm is going off, like they're calling for the fire trucks.
So this is an issue.
And it's happening right in the ovarian tissue, right in your ovaries, right in your ovaries.
So we have to deal with this inflammation, these fires. So where do the fires start elsewhere in the body that just add compound to this issue?
Think of it like water in a bucket.
If you have PCOS, you could genetically be more prone to this issue. Think of it like water in a bucket. If you have PCOS, you could genetically
be more prone to developing inflammation. It's not fair. I didn't say it was fair,
but there's stuff we can do. But on top of that, water in a bucket, how much other inflammation
are we adding to this bucket until the bucket overfloweth and now we have serious issues?
Well, inflammation can happen a lot of places. Micome problems, gut issues, gas bloating, constipation, diarrhea,
ulcers, heartburn, H. pylori, worms, anything, amoebas, that can all affect it. Pathogens,
stealth and overt, so maybe bacteria, viruses, Lyme, doesn't matter. All of those things, when you get the flu,
right? When you cut your arm and it gets red and it hurts and maybe a little swollen,
that's inflammation. Now, inflammation is swooping in to do its job, get rid of the infection,
help to start the healing process, completely normal. Completely normal. When I have the flu,
I want my immune system pissed. I want my immune system to swoop in and get rid of whatever gave
me the flu, the flu virus. But then I want it to stop in a healthy manner. I want it to resolve
and heal in a healthy manner. But what if it doesn't? What if it can't? What if the Morse
code in my immune system isn't working very well? And so now I constantly have this low-grade inflammation there.
Foods.
Did you know that foods, the foods that you eat over and over and over again could be
causing lower high-grade inflammation?
If you know without a doubt, you should not be eating dairy because every time you eat
dairy, it gives you heartburn or it upsets your stomach, gives you gas, makes you bloated,
but you eat it anyway because you really like it.
Like you really like cheese.
You will never give up yogurt. Ice cream is your savior. You're inducing inflammation every single
time. If you're allergic to a food or sensitive to a food and it's pretty overt like that, what
are you doing? Just be aware. Toxicants and chemicals. This can be a really hard one for
people. In fact, I just saw a TikTok video saw, um, a, a Tik TOK, uh, video. It was
a cute Tik TOK about like couples and relationships. So one of the suggestions was to wear
a sexy perfume at night. And I was like, ah, now you're sleeping in all that synthetic fragrance,
all that valley, right? All that plast, the plasticizer and stuff in it. And, uh, it's,
it's an endocrine disrupting chemical. There are obviously less toxic chemicals out there and less toxic fragrance. Maybe your room
is filled with beautiful glass candles. Your house has plugins. Your car has things hanging
off the rear view mirror. Your detergent smells amazing. Your dryer sheets are like a spring day.
All of those chemicals, that fragrance, the stuff you put on your skin,
the stuff you clean your counters with, what you spray all over your garden in the summer and the
spring, that adds up. It adds up and it can cause inflammation over time in the body. And in fact,
a lot of those can cause inflammation immediately. I mean, if you've ever come in contact with some
sort of mildly irritating chemical and your skin itches or your eyes water
or your nose is runny or your throat burns. Now imagine you do that over and over and over again.
Please be very careful. Read labels, switch to healthier options. Having excess adipose tissue,
I already talked about, and how it can make its own inflammatory chemicals called cytokines.
Injury. We see this, right? With injury, you injure yourself, whether you trip,
you fall, sports, car accident, whatever it is. If you have a normal healing process, fantastic.
But what happens if you don't? Or what happens if you keep re-injuring yourself? What happens
if it's something very serious, like a head trauma that can take a really long time to heal?
And a lot of people don't actually know how to heal a head
trauma traumatic brain injury and so they're still struggling years later inflammation low
grade inflammation or even moderate to high grade inflammation stress trauma big t's and little t's
i did not coin that i have heard it several times over though i apologize i don't know who the
originator of big t's and little t's are but it's your big traumas and your little traumas. They add up. How are you coping with those? Are
you coping with those? Are you working through those? Genetically prone, we talked about sleep
and circadian rhythm dysfunction. As humans, we are meant to be up with the sun and down with the
dark. And boy, we've messed that up, haven't we? We are on synthetic light all the time. We're on
our phones all the time. You may be watching this on your computer at night. So we've messed that up, haven't we? We are on synthetic light all the time. We're on our phones all the time.
You may be watching this on your computer at night.
So you've got that light shining into your eyes.
You maybe are on TV watching shows,
your tablet reading,
and it's that bright synthetic light that's affecting sleep and melatonin
and healing and repairing.
You get up in the morning,
immediately go to your phone.
You haven't been outside in days.
Keep these things in mind. This can all really affect how inflammation does or doesn't play out
in your body and a lot of other things. So let's talk about inflammation and visceral adiposity.
So visceral obesity. So weight gain and obesity are not diagnostic criterias for PCOS. However,
it is a super common feature. 25 to 75% of those with PCOS have weight gain. That's a complaint.
They come to their doctor.
They're like, oh my gosh, I'm gaining weight or outright overweight or obese. So insulin resistant PCOS, IRs, insulin resistant, tend to have that visceral, that in, right around the organs as we
talked about. And as I've said, that creates that low grade inflammation automatically.
With that, with that, so this one, in the inflammation of visceral obesity,
we've talked about quite a bit. Another form of inflammation down in the ovaries is called
endoplasmic reticulum stress in the ovaries. In our cells, we have mitochondria. You learned
about mitochondria a long time ago in school.
You learned that they are cellular powerhouses, but maybe you forgot about the endoplasmic
reticulum. So I've got it circled there. So mitochondria float around. We love our mitochondria.
They make ATP, but endoplasmic reticulum are super important for how your cell functions.
It's also super important for how you do or don't make a lot of hormones.
Your hormone first stop is in the mitochondria.
That's the first step, actually.
Then most all of them move over to the endoplasmic reticulum and finish out there.
You want to make a testosterone, you start in the mitochondria, you finish in the endoplasmic
reticulum, and it goes out in circulation.
Cortisol is the one that goes out to the endoplasmic reticulum, comes back to the mitochondria,
and then goes out to the endoplasmic reticulum, comes back to the mitochondria, and then goes out in circulation.
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