Speaker 1: Hi, my name's logan. I'm a transgender man. I use
Speaker 1: he hymn pronouns, and I have PCOS. My symptoms first
Speaker 1: started really appearing when I hit puberty. My periods would
Speaker 1: last a week on average, and they were very heavy.
Speaker 1: The cramps would be so bad that I couldn't walk,
Speaker 1: I couldn't sleep. I would just lay awake at night
Speaker 1: in agony, despite taking pain medications. I also had very
Speaker 1: severe acne, and I had a lot of excess body
Speaker 1: and facial hair. If I didn't shave or pluck my hair,
Speaker 1: I could actually grow like this scraggly little chin beard,
Speaker 1: which was very affirming to me as a young trans
Speaker 1: masculine person. That was probably the only benefit of having
Speaker 1: PCOS was the masculinizing features. By the time I was nineteen,
Speaker 1: my periods became even more painful, if that was possible,
Speaker 1: and even more irregular. At one point, I went ten
Speaker 1: months without a period. December twenty eighteen is when I
Speaker 1: first experienced assist bursting. I was sitting in a college
Speaker 1: math final at the time, and I remember being in
Speaker 1: so much pain from my abdomen that I could barely breathe.
Speaker 1: I managed to finish the final, but I could hardly
Speaker 1: walk because of the pain, so I was rushed to
Speaker 1: the er. When we got there, I was not treated well.
Speaker 1: They started off by accusing me of faking my pain
Speaker 1: to get opioids, but soon after they thought that it
Speaker 1: could be appendicitis. I had to get blood drawn and
Speaker 1: a cat scan. They actually ended up bursting one of
Speaker 1: the veins in my arm like trying to do the
Speaker 1: die for the cat scan, so that was also not
Speaker 1: a fun experience. When the doctor finally came in to
Speaker 1: give me a diagnosis, or so I thought, all he
Speaker 1: really told me was your appendix is fine, but you
Speaker 1: have multiple cysts on both your ovaries, so just go
Speaker 1: on birth control, and then I was dismissed right after
Speaker 1: with no diagnosis. The next year that followed, I had
Speaker 1: to get a lot of blood work and scans done,
Speaker 1: but no one seemed to understand what was wrong with me.
Speaker 1: I started birth control but immediately became extremely depressed and suicidal.
Speaker 1: My body reacted so poorly that I had to quit
Speaker 1: after like a month. It was actually very terrifying how
Speaker 1: it changed my mental state. And once I stopped the
Speaker 1: birth control, I really wasn't given any other options. For treatment.
Speaker 1: At some point, a doctor pulled me to the side
Speaker 1: and said, I looked at your records and I'm going
Speaker 1: to formally diagnose you with PCOS. You have elevated testosterone,
Speaker 1: facial hair, irregular periods, and multiple cysts on both ovaries.
Speaker 1: I'll never forget her telling me that I was lucky
Speaker 1: that I had lean PCOS, which basically meant you have PCOS,
Speaker 1: but at least your skinny. Once again, I was told
Speaker 1: my only options for treatment were birth control, which did
Speaker 1: not work before, or to get pregnant. Much to my horror,
Speaker 1: By this time, I was aware that I was transgender,
Speaker 1: and I told her birth makes me suicidal, so she said,
Speaker 1: in that case, I should just go to therapy and
Speaker 1: go on a diet. I was twenty years old and
Speaker 1: one hundred and twenty five pounds at the time. Needless
Speaker 1: to say, the diet didn't help. I lived in chronic
Speaker 1: pain for the next few years, with both my physical
Speaker 1: and emotional states causing me a lot of harm. It
Speaker 1: wasn't until I decided to start testosterone for my gender
Speaker 1: dysphoria that I actually felt like myself again. As a
Speaker 1: result of taking testosterone, my period stopped. My mental state stabilized,
Speaker 1: and I was happy and pain free for the first
Speaker 1: time in a very long time. I remember bringing this
Speaker 1: up to my new doctor and her telling me some
Speaker 1: bodies just function better on different hormones. I've now been
Speaker 1: living without PCOS symptoms for the past three years, and
Speaker 1: the quality of my life has greatly improved. I'm a bioengineer,
Speaker 1: and it really breaks my heart that this is the
Speaker 1: state of medical care for people who menstraight. I experienced
Speaker 1: a lot of sexism and a lot of transphobia throughout
Speaker 1: the whole process. All the assumptions doctors made about me
Speaker 1: at the time were made through these heterosexual cisgender lenses.
Speaker 1: They assumed that I didn't want to look masculine, that
Speaker 1: I'd eventually get pregnant, and that only birth control and
Speaker 1: estrogen based pills would work for my body. But this
Speaker 1: was never the case, and I suffered so much as
Speaker 1: a result. Transgender people are often left out of these conversations,
Speaker 1: and I think it's important for people to know just
Speaker 1: how distressing it can be to have your pain and
Speaker 1: your identity dismissed by the medical field.
Speaker 2: Logan, thank you so much for sharing your story with us.
Speaker 2: It really is so meaningful and important to get to
Speaker 2: hear these stories of like what it is actually like
Speaker 2: to live with PCOS. I think, really it really helps
Speaker 2: so much.
Speaker 3: Yeah, it really provides so much context for us, for
Speaker 3: everyone listening. And thank you so much for sharing your
Speaker 3: story with us.
Speaker 4: Hi, I'm Aaron Welsh and I'm Erin Allman Updike and.
Speaker 2: This is this podcast will kill you.
Speaker 4: Welcome to PC long awaited.
Speaker 2: I feel like so long awaited. I mean, I wonder
Speaker 2: I didn't do this search, but I wonder if you
Speaker 2: like searched our email. Oh gosh, what the first suggestion
Speaker 2: for PCOS would be?
Speaker 3: It had to be years ago, and probably probably even
Speaker 3: before we did endometriosis, which was how many years ago now,
Speaker 3: long time?
Speaker 2: Twenty nineteen?
Speaker 4: Was that?
Speaker 2: No, No, I don't remember. I later, I don't remember either.
Speaker 4: It's fine, and it's been a minute.
Speaker 2: It's been a minute.
Speaker 3: And PCOS has been on our radar since then and before.
Speaker 3: And I am thrilled for this episode and also honestly
Speaker 3: embarrassed by how little I knew. When I thought that
Speaker 3: I knew, I I was diagnosed with PCOS in twenty thirteen,
Speaker 3: I remember, Yeah, and I went through all of med
Speaker 3: school and all of residency. So I thought that I
Speaker 3: had a pretty good handle on PCOS. I learned so
Speaker 3: much Aarin.
Speaker 2: Yeah, I same, same. I mean, I do not have
Speaker 2: PCOS as far as I know, But I thought I
Speaker 2: thought I was like, oh, yeah, I know what this is.
Speaker 4: Yeah, my gosh.
Speaker 2: Yeah, And so like I'm just so I think that
Speaker 2: this was a moment where I was so I'm so
Speaker 2: grateful that we get to do this podcast.
Speaker 5: Same where because part of it selfishly is like, oh
Speaker 5: I feel like I know more about this now, Like
Speaker 5: I there were I had all these misconceptions.
Speaker 2: There were things that I finally realized. But I think
Speaker 2: also like this is so many people have similar misconceptions.
Speaker 4: I know exactly, Like it's never just us.
Speaker 5: It's never just us. Yeah, so we're really excited. Yeah
Speaker 5: maybe sometimes it is.
Speaker 2: Just maybe it is just us. But in any case,
Speaker 2: in any case, I'm excited. But before we get into
Speaker 2: the full picture of PCOS, it's quarantin any time time,
Speaker 2: who are we drinking?
Speaker 4: We're drinking under revision. Those are Brackett.
Speaker 2: Watching us listening, Yes, under revision Because truly, like I
Speaker 2: feel like our our perception of this is constantly changing
Speaker 2: and needs to change in many ways to deliver better
Speaker 2: care and better empathy and awareness.
Speaker 4: So we'll get into So tell us first, are what's
Speaker 4: in under Revision.
Speaker 2: It's it's it's a place Brita version and it's so good.
Speaker 2: It's lavender syrup and lemon juice and club soda and
Speaker 2: it's like a little lavender lemona fresh and relaxing.
Speaker 3: Yeah, we'll post the full recipe on our website, This
Speaker 3: podcast will kill you dot com. We'll post a video
Speaker 3: of Aaron Welsh making it.
Speaker 4: Sorry.
Speaker 3: Yeah, we're gonna try on our social media's like Instagram
Speaker 3: and the TikTok and the Facebook, et cetera. We're on
Speaker 3: Blue Sky as well. So if you're not following us,
Speaker 3: you should consider doing that. If you haven't yet rated
Speaker 3: and reviewed and subscribed to our podcast on your favorite podcatcher,
Speaker 3: iHeart Podcasts, Apple Podcasts, Spotify, we'd love it if you
Speaker 3: do that. If you're not yet subscribed to the exactly
Speaker 3: right YouTube network channel, consider doing that.
Speaker 2: We're there just a gentle recommendation, a nudge.
Speaker 4: A nudge in the right direction, and.
Speaker 2: We have it exactly right direction. Sorry, thank you, thank you.
Speaker 3: And Finally, we have a website. It's called this podcast
Speaker 3: will Kill You dot com and on it you can
Speaker 3: find merch you can find Patreon, you can find bookshop
Speaker 3: dot org affiliate accounts, and a Goodreads list, and Bloodmobile
Speaker 3: who does our music, and all of our sources, and
Speaker 3: so much more, so much more.
Speaker 2: And that was great, and I think there's nothing else
Speaker 2: to cover except PCOS. So let's take a break and begin.
Speaker 4: Okay, can't wait.
Speaker 3: PCOS stands for polycystic ovarian syndrome, which really makes it
Speaker 3: sound like it's a disease where you have cysts on
Speaker 3: your ovaries. This should be pretty straightforward. It's not that, Arren,
Speaker 3: not that, not that.
Speaker 2: That was my misconception Number one. I was like, surely
Speaker 2: the name must be a clue as to what's going
Speaker 2: on here.
Speaker 4: Not even really a good clue at all.
Speaker 3: Actually, Yeah, what PCOS really is is an endocrine disorder,
Speaker 3: which means it's a disorder of our hormones. And not
Speaker 3: just like one or two of our hormones. No, no,
Speaker 3: today we're going to get to talk about almost all
Speaker 3: of the hormones that we use and have in our
Speaker 3: bodies and their effect on all of our body systems. Okay, Yeah,
Speaker 3: there is not a single test that we can do
Speaker 3: to diagnose PCOS, but rather there are a list of criteria, okay,
Speaker 3: and you have to fulfill two of three of these
Speaker 3: criteria to earn I guess the diagnosis of PCOS. And
Speaker 3: this list underscores some, though not all, of the possible
Speaker 3: And I'm going to put this in quotes symptoms because
Speaker 3: we're going to get into it, but some of the
Speaker 3: possible symptoms of PCOS. And so I thought that that's
Speaker 3: where we would start, is how we actually diagnose PCOS.
Speaker 3: And then we'll talk about what we know about what
Speaker 3: PCOS means in terms of the risks of various chronic diseases.
Speaker 3: And then we can get as deep or stay as
Speaker 3: shallow as you want in terms of what we know
Speaker 3: about the nitty gritty path of physiology of what's causing this.
Speaker 2: How much do we actually know about the nitty gritty
Speaker 2: of the path of physiology that's causing.
Speaker 4: This, Aaron, we know both a lot and so little.
Speaker 2: I mean, that's typical, Yeah it.
Speaker 4: Is, isn't it. And then we'll talk about how we
Speaker 4: treat it.
Speaker 3: And my goal is to do this in twenty minutes,
Speaker 3: so we'll see if that's gonna happen.
Speaker 4: I think, ah, it won't. It's quite a lofty goal.
Speaker 4: I know.
Speaker 3: You should see all the words on a page. So
Speaker 3: there has been fluctuation over the years over these diagnostic criteria,
Speaker 3: but at this point there's pretty well established guidelines on
Speaker 3: how we diagnose PCOS. So to make this diagnosis, you
Speaker 3: need two out of three of the following criteria. One
Speaker 3: is hyperandrogenism, and we'll talk about what that means. And
Speaker 3: this can be either clinical so symptoms that you can
Speaker 3: see on a person or biochemical, so looking at lab tests,
Speaker 3: you have to have a ligomenorreea or a menorrhea so
Speaker 3: few periods or not having any periods at all, and
Speaker 3: polycystic ovarian morphology. So you need two out of three
Speaker 3: of those. So let's talk about what those actually mean,
Speaker 3: like what they would look like right right, English. So,
Speaker 3: hyper androgenism means an elevated amount of androgens, which are
Speaker 3: steroid hormones. We often think of testosterone, and testosterone is
Speaker 3: one of the androgens, but there's a lot of others,
Speaker 3: DHA andristino, dione, there's a whole bunch, okay, and so
Speaker 3: you can determine whether a person has what is considered
Speaker 3: hyper androgenism by measuring the levels of those hormones in
Speaker 3: a person and comparing that to what we see in
Speaker 3: typical females. And this is again we're talking about people
Speaker 3: with ovaries here, and that is entirely the focus of
Speaker 3: PCOS at this point.
Speaker 4: Asterix abound.
Speaker 2: Quick question. Okay, when you are let's say you are
Speaker 2: being tested for these hormone levels, what does that test involve?
Speaker 3: Those are If you're testing for hormone levels, it's going
Speaker 3: to be blood tests. What exact hormones people are going
Speaker 3: to test for can vary depending on who is doing
Speaker 3: that test. One of the important things is to make
Speaker 3: sure that you're doing enough testing to rule out other
Speaker 3: androgenic disorders. Because your adrenals produce androgens. There's other like
Speaker 3: known disorders where we know, like, oh, you have a
Speaker 3: deficiency in say this enzyme that produces a specific clinical
Speaker 3: syndrome that's different than PCOS. Okay, and so you have
Speaker 3: to do enough of the blood tests to make sure
Speaker 3: that you're ruling out these other things. And then if
Speaker 3: you see still an increase in androgens, and again this
Speaker 3: is already where we can get some variation, because you
Speaker 3: might have an increase, you might not have an increase.
Speaker 3: But this is just one possible criteria, and you can
Speaker 3: look at a number of different androgens.
Speaker 5: So that's one. I already have so many questions. I know, Okay,
Speaker 5: so that like where it where? What is the source
Speaker 5: of the excess androgens?
Speaker 3: You're jumping so far ahead? Okay, Okay, there, we'll get there.
Speaker 4: We'll get there.
Speaker 3: Ultimately, the main source of the extrass androgens is the
Speaker 3: over but the question of why is yeah, okay, but
Speaker 3: ultimately the ovaries are producing excess androgens.
Speaker 2: And I just I swear two more quick questions because
Speaker 2: I'm trying to get a sense of what elevated means. Yeah,
Speaker 2: so is this how how much do hormones fluctuate during
Speaker 2: the day, during the range, during the year, et cetera.
Speaker 2: And so then how much is excess? How is excess determined?
Speaker 2: Or like how is greater than average determined? What's is
Speaker 2: there a standard deviation? Like what's the vibe?
Speaker 4: This is a great question here.
Speaker 3: There's not like a number cut off necessarily, So every
Speaker 3: lab that you do a lab test at is going
Speaker 3: to have there. What is called like normal range or
Speaker 3: typical range, and for hormones like testosterone or DHA or
Speaker 3: estrogen or progesterone or any of those, they're going to
Speaker 3: have a normal range for females and they're going to
Speaker 3: have a normal range for males. And so if it
Speaker 3: is higher than that normal range for females, then that
Speaker 3: would be consideredhyperandrogenism. And that could be if you're looking
Speaker 3: at free or total testosterone, or it could be one
Speaker 3: of these other hormones. I don't have like exact numbers,
Speaker 3: and you're right that it can vary day to day.
Speaker 3: It can vary during the time of day as well,
Speaker 3: So again this can get quite complicated. Okay, it doesn't
Speaker 3: have to be bio It's okay, don't all. I love
Speaker 3: your questions. It does not have to be biochemical evidence, though.
Speaker 3: We also can see what's considered clinical evidence of hyper androgenism,
Speaker 3: and that usually there's three main things that we think of.
Speaker 3: Acne usually more severe acne, sometimes cystic acne but not necessarily,
Speaker 3: androgenic alopecia aka scalpel like male pattern hair loss, and hersitism,
Speaker 3: which I always have to look up how to pronounce
Speaker 3: because I'm.
Speaker 2: Glad that you said that first, because I would have
Speaker 2: gotten it wrong.
Speaker 3: Hersaitism, which is hair growth like coarse, thick hair growth
Speaker 3: that specifically grows to longer than five millim so not
Speaker 3: just tiny tiny little hairs in androgen dependent areas, So
Speaker 3: that means places like the under arms, the pubic area,
Speaker 3: the face. And this is a kind of tricky one
Speaker 3: because there's a grading scale that in theory one should
Speaker 3: use to determine how much would be considered excess or
Speaker 3: like hersaitisms truly, and there's also going to be like
Speaker 3: racial and ethnic variation in hair patterns to begin with,
Speaker 3: but that is also one of the possible clinical criteria.
Speaker 3: So that's all just hyperandrogenism. That's one thing that someone
Speaker 3: might have to put them on this list of possible pcos.
Speaker 3: The second is ovulatory dysfunction, which means people either aren't
Speaker 3: ovulating at all and then therefore they're not having any menses,
Speaker 3: or they're ovulating infrequently or irregularly, and so they're having
Speaker 3: very infrequent or irregular menstrual cycles. Exactly how infrequent or
Speaker 3: like how far apart they have to be or how
Speaker 3: irregular depends in part on how far you are from
Speaker 3: menarch or that first menstrual period, because it's quite typical
Speaker 3: in the first few years to have irregular menstrual cycles. Okay,
Speaker 3: but if you are more than three years after your
Speaker 3: first menstrual cycle, than anything less than eight per year
Speaker 3: or greater than thirty five days apart would be considered
Speaker 3: a ligomin arehea or having few menstrual cycles. But that's again,
Speaker 3: so that's that's one, so ovulatory dysfunction. And then the
Speaker 3: third and final is polycystic ovarian morphology, which does not
Speaker 3: really mean that you have a bunch of cysts on
Speaker 3: your ovaries, but means that if you look on ultrasound
Speaker 3: in the ovaries, you see a bunch of and by
Speaker 3: a bunch, I mean twenty or more visible follicles that
Speaker 3: are arrested in an early stage of development, so we're
Speaker 3: born in with all, if you have ovaries, your ovaries
Speaker 3: have as many eggs in there as they're going to have.
Speaker 3: And typically, in response to these hormone cycles, every month,
Speaker 3: one like multiple follicles start to mature, but then one
Speaker 3: takes over matures completely and then is released during ovulation.
Speaker 3: And what happens in PCOS is that multiple follicles start
Speaker 3: to grow and then grow to a certain point, but
Speaker 3: then are arrested in their development without ever having one
Speaker 3: that takes over and is released, which is why you
Speaker 3: have a lego or a menoreea because you're not ovulating.
Speaker 3: And then it's also why you have so many of
Speaker 3: these kind of follicles that are arrested at a stage
Speaker 3: in development, that is, before they get to ovulation.
Speaker 2: Okay, So you've got a bunch of these like not
Speaker 2: fully uh developed, developed follicle matured follicles just hanging out
Speaker 2: at the ovary and causing like little grape clusters.
Speaker 4: Yeah, they look like little grape clusters. Okay.
Speaker 3: Sometimes on ultrasound you might not see specific follicles, but
Speaker 3: you would have an overall larger volume, like greater than
Speaker 3: ten millimeters volume without having one dominant follicle, because if
Speaker 3: you have just one that's burst or ready for ovulation,
Speaker 3: that you can get quite large large.
Speaker 4: Okay, Okay.
Speaker 3: Now, one thing that's new in the most recent guidelines
Speaker 3: from twenty twenty three is that you don't necessarily have
Speaker 3: to do an ultrasound to look for those polycystic ovaries.
Speaker 3: You also could diagnose polycystic ovarian morphology by looking at AMH,
Speaker 3: which is another hormone that you would check via a
Speaker 3: blood test that we've talked about I think in our
Speaker 3: infertility episodes or n menopause. Not sure, Yeah, I know
Speaker 3: we mentioned it in menopause as well, But this is
Speaker 3: a hormone that relates to like how many follicles are
Speaker 3: still in existence in your ovary kind kind of a thing,
Speaker 3: and having an elevated level of AMH is suggestive of PCOS.
Speaker 3: But again here there's not like an exact cutoff value
Speaker 3: yet for this, which is interesting in and of itself.
Speaker 3: So that's how we diagnose it. You got to have
Speaker 3: two out of those.
Speaker 2: Three, Okay, so either you have this hyperandrogenism infrequent or
Speaker 2: no periods.
Speaker 5: And polycystic Yeah, psychology, Yeah, in the name, yeah, in
Speaker 5: the name.
Speaker 4: I was like, what's the third?
Speaker 3: And so because there are these three different criteria and
Speaker 3: you only need two out of three to have a diagnosis,
Speaker 3: it leads to four different what are called phenotypes of PCOS.
Speaker 3: So one of the options is that you have all three,
Speaker 3: You meet all three of these criteria, and that would
Speaker 3: be called phenotype A. The second option is that you
Speaker 3: have evidence of hyper androgenism and evidence of ovulatory dysfunction
Speaker 3: without having polycystic ovaries.
Speaker 4: We'll call them.
Speaker 3: Polycystic ovaries, they're not sis, and that would be phenotype B,
Speaker 3: and those two together are called classic PCOS, and they
Speaker 3: account for an estimated two thirds of people with PCOS.
Speaker 3: So two thirds of people with PCOS will have evidence
Speaker 3: of hyper androgenism either clinical or online tests, and they'll
Speaker 3: have ovulatory dysfunction with or without having polycystic ovarian morphology
Speaker 3: on ultrasound. The third phenotype phenotype C, someone will have
Speaker 3: hyper androgenism and on ultrasound polycystic ovarian morphology, but without
Speaker 3: necessarily having any issues in terms of their ovulation, so
Speaker 3: not having aligomin area. And then phenotype D is ovulatory
Speaker 3: dysfunction and polycystic ovarian morphology but no evidence of hyper androgenism.
Speaker 5: All right, Okay, Okay, why it's a great question.
Speaker 3: Okay, So just looking at all of those that there's
Speaker 3: a there's a y question, and then there's a huge
Speaker 3: part that's missing already, okay in these diagnostic criteria, because
Speaker 3: those criteria give us a lot of insight into some
Speaker 3: of the symptoms as well as some of the consequences
Speaker 3: of PCOS. Right, So, an ovulation, which can happen very
Speaker 3: commonly in PCOS, can result in infertility or reduced fertility,
Speaker 3: and PCOS is the major cause is estimated to be
Speaker 3: like the number one cause of an ovulatory infertility. So
Speaker 3: if you're not ovulating and you can't get pregnant when
Speaker 3: you want to be pregnant, PCOS is the number one
Speaker 3: cause of that. In addition, this an ovulation also leads
Speaker 3: to an increased risk of endometrial cancer down the line.
Speaker 3: And that's because your uterus, because of the hormones that
Speaker 3: are floating around, is out here like getting ready to
Speaker 3: have an egg implant. It's getting ready, it's getting ready,
Speaker 3: it's getting ready. That egg never comes. You never menstrate.
Speaker 3: Your uterus lining is proliferating this whole time, and that
Speaker 3: proliferation increases the risk of cancer in this continually proliferating tissue. Okay,
Speaker 3: the hyperandrogenism that we see in PCOS that we can
Speaker 3: see may or may not be associated with symptoms that
Speaker 3: are undesirable, right, It depends on someone's perception of what
Speaker 3: those symptoms are. Male pattern hair growth or hair loss
Speaker 3: may or may not be something that is distressing to
Speaker 3: someone acne. Most people are not a fan of acne.
Speaker 4: But this, all of.
Speaker 3: These definitions are missing one of the huge, very clear,
Speaker 3: well defined major factors of PCOS, and that is its
Speaker 3: relationship to insulin resistance. Yeah, so insulin resistance leads to
Speaker 3: glucose intolerance, and that puts people at risk for type
Speaker 3: two diabetes as well as a whole bunch of other
Speaker 3: metabolic complications hyperlipidemia. So having elevated cholesterol levels, that puts
Speaker 3: you at risk for cardiovascular disease, It puts you at
Speaker 3: risk for hypertension, and so much more. And PCOS also
Speaker 3: gets quite a lot of attention as it relates to obesity,
Speaker 3: which I always put in quotes because obesity is it's
Speaker 3: considered a disease in medicine that is defined entirely based
Speaker 3: on BMI, and BMI is not an indicator of health. Right,
Speaker 3: Elevated BMI is associated with PCOS, but whether this is
Speaker 3: cause or consequence is very much still up for debate.
Speaker 2: Which I feel like is a lot of some of
Speaker 2: the symptoms associated or that are prevalent with PCOS. So consequence, yeah.
Speaker 3: Yeah, but all of these and here's what's really important
Speaker 3: about that is that all these other symptoms, and there
Speaker 3: are a lot so like increased risk of insulin resistance,
Speaker 3: risk for type two diabetes, risk for hyperlipidemia. Even people
Speaker 3: who have PCOS are also at an increased risk for
Speaker 3: obstructive sleep apnea.
Speaker 4: We don't know the.
Speaker 3: Mechanism there, but all of those risks increase regardless of BMI.
Speaker 3: They exist regardless of BMI. We know that, or we think,
Speaker 3: at least from the data that we have so far,
Speaker 3: which is mostly in mouse models, that PCOS might be
Speaker 3: related to changes in adipose tissue, like the way that
Speaker 3: your adipose tissue responds to insulin or things like that,
Speaker 3: and have how it like uptakes glucose and things like that.
Speaker 3: But all of the other complications and metabolic complications in
Speaker 3: PCOS are prevalent regardless of BMI, and in like BMI
Speaker 3: matched case control studies, they are elevated in PCOS regardless
Speaker 3: of BMI, just like in people without pcos in some cases,
Speaker 3: and elevated BMI can also put you at higher risk
Speaker 3: for some of these other metabolic complications. So again, what
Speaker 3: is the cause and what is the consequence?
Speaker 4: We don't know.
Speaker 3: What we do know, and what is prevalent enough that
Speaker 3: it has made it into the twenty twenty three guidelines.
Speaker 3: Is the very real problem of fat shaming that happens
Speaker 3: in PCO and weight stigma, like enough so that the
Speaker 3: awareness of this fat shaming and stigma is in the
Speaker 3: PCOS guidelines of Like you need to be aware of
Speaker 3: this if you're a clinician and not do it. Yeah,
Speaker 3: but like you said, we do not know exactly how
Speaker 3: this metabolic dysfunction happens at the beginning, Like what are
Speaker 3: the core causes of it?
Speaker 2: And how does how do other hormones play into this? Oh,
Speaker 2: my gosh, Aaron, what's what's what's the timeline? The sequence?
Speaker 2: The cascade is a by.
Speaker 3: Step If I could tell you a step by step cascade,
Speaker 3: I would have a lot more clarity as to what
Speaker 3: the heck is going on. But I can give you
Speaker 3: some more detail, Okay, to kind of understand a lot
Speaker 3: of what's going on in PCOS. We can first understand
Speaker 3: what's called our HPO axis. This is our hypothalamic pituitary
Speaker 3: ovarian axis or gonadal access because you have one if
Speaker 3: you have testies too, so in your hypothalamus you are
Speaker 3: releasing hormones there's a part in your brain you're releasing hormones.
Speaker 3: The one that is important in PCOS is called gnatotropin
Speaker 3: releasing hormone, and it is.
Speaker 4: Being pulsed out. It is normal.
Speaker 3: It is typical in our brains that it's not being
Speaker 3: released all the time, but we pulse it out in phases.
Speaker 3: Your brain is like, yep, give a little bit, Yep,
Speaker 3: give a little bit. Its job is to travel to
Speaker 3: our petuitary and tell our petuitary, which is another part
Speaker 3: of our brain, to secrete other hormones lutinizing hormone LH
Speaker 3: and follical stimulating hormone FSH. We've talked about these in
Speaker 3: our infertility our pregnancy episodes. These two hormones job is
Speaker 3: to travel through our bloodstream, go to our ovaries and
Speaker 3: modulate the production of estrogen and progesterone and make our
Speaker 3: ovaries mature one follicle release it and ovulate. Right, this
Speaker 3: whole system, our HPO axis works on a system of
Speaker 3: both positive and negative feedback loops. Right, So one part
Speaker 3: of our brain tells another part of our brain tells
Speaker 3: our ovaries, and those hormones go back to our brain
Speaker 3: and they're like, hey, we're here, so calm down.
Speaker 4: Right, yeah, yeah, yeah.
Speaker 3: In PCOS, there is a wrench in this system. What
Speaker 3: exactly the first wrench is we don't know. So we
Speaker 3: know that the pulsatility of this gnatotropin releasing hormone GnRH
Speaker 3: in PCOS is increased, so we see more and more
Speaker 3: frequent pulsatility of GnRH from our hypothalamus. What that does
Speaker 3: is it tells our pituitary ooh, keep going, keep going,
Speaker 3: keep going, and actually leads to a disruption in the
Speaker 3: LH versus FSH ratios.
Speaker 4: Oh.
Speaker 2: And so instead of like it being okay, now ovulate,
Speaker 2: it's like, oh maybe maybe maybe maybe it's just like
Speaker 2: less of a strong message.
Speaker 3: Yeah, And the message is like mature, mature, mature, mature, mature, mature,
Speaker 3: A bunch of follicles, bunch of follicals. But no, there's
Speaker 3: no ovulation, there's no release, there's no release signal. Right,
Speaker 3: And that because that LAH is then going to our
Speaker 3: ovaries and it's being like make make make androgens, make androgens,
Speaker 3: make adrogens, then there's also something else going on because
Speaker 3: that hyper agigen secretion should negative feedback onto our hypothalamus
Speaker 3: and be like hey stop, but that negative feedback is impaired.
Speaker 4: We don't exactly know why. Hmmm.
Speaker 3: Then okay, here's where it gets even more complicated erin Okay, okay,
Speaker 3: where does insulin resistance play into this?
Speaker 4: That's what I'm trying to figure out.
Speaker 3: We know, yeah, that insulin resistance tissue level. Insulin resistance
Speaker 3: leads to an increase in insulin production, right, because if
Speaker 3: your body is trying to red glucose, insulin is in
Speaker 3: charge of that. And if your tissues aren't responding to insulin,
Speaker 3: insulin is binding through the receptors it's supposed to, but
Speaker 3: it's not doing its job, so you can't collect that glucose.
Speaker 3: Then your body's going to make more insulin because it's like, hey,
Speaker 3: there's too much glucose floating around. We need more insulin,
Speaker 3: more insulin, more insulin. That hyper insulinemia feeds back onto
Speaker 3: the ovaries and tells them, by a reason I don't understand,
Speaker 3: to make more androgens.
Speaker 2: Okay, I mean, okay, but no, I don't understand exactly.
Speaker 4: No, we don't know why.
Speaker 3: So in short, we know that all of these feedback
Speaker 3: loops are sort of not working the way that they
Speaker 3: would directly.
Speaker 2: In some way.
Speaker 4: Yeah, there's more.
Speaker 3: And more evidence because we used to think like, oh,
Speaker 3: it's just the ovaries, and there's some evidence in like
Speaker 3: mice and rats that like disruption at the level of
Speaker 3: the ovary, just like a tendency to excess androgen secretion
Speaker 3: to begin with, can produce things like polycystic ovarian morphology. Okay,
Speaker 3: but it again doesn't account for the lack of this
Speaker 3: negative feedback loop. It doesn't necessarily account for this insulin
Speaker 3: resistance piece of it. So there's more evidence that these
Speaker 3: other groups of hormones that act more in our brains
Speaker 3: called kiss peptins and other like other types of hormones
Speaker 3: as well are likely involved. So I guess the point
Speaker 3: of all of this is to say, a number one
Speaker 3: it's complicated.
Speaker 4: Yeah, and b number one.
Speaker 5: While we know a lot number two or be number
Speaker 5: one whatever, A number one, it's complicated, be number two.
Speaker 3: We know a lot about the features of these disruptions
Speaker 3: increase GnRH pulsatility, increased androgens, insulin resistance leading to more
Speaker 3: increased androgens. We also see like a decrease insects hormone
Speaker 3: binding globulin because of these androgens. So like there's all
Speaker 3: these feed back loops that are very well documented and
Speaker 3: drawn in all these papers, But we do not know
Speaker 3: what the first underlying issue really is, right, which means
Speaker 3: that all of our treatments that we have are addressing
Speaker 3: individual parts of the issue but not coming close to
Speaker 3: like curing anything or really getting to like one drug
Speaker 3: or one mechanism fixing this cascade. So do we think
Speaker 3: that it is one mechanism? That is an excellent question.
Speaker 3: Arin no idea, Okay, especially because when you think of
Speaker 3: all of these different phenotypes, right, I said that there
Speaker 3: are four different phenotypes. They also are associated with like
Speaker 3: differential risk in things like insulin resistance. Okay, So types
Speaker 3: A and B that like classic PCOS picture, something like
Speaker 3: eighty percent of people with this phenotype will have evidence
Speaker 3: of insulin resistance and therefore might be at high risk
Speaker 3: of things like diabetes. Phenotypes C we see still a
Speaker 3: significantly increased insulin resistance, but like sixty percent compared to
Speaker 3: eighty percent. And in phenotype D, which is the one
Speaker 3: where people have no clinical hyperandrogenism, about forty percent of
Speaker 3: them we see insulin resistance. But in all of these
Speaker 3: the incidence of type two diabetes and is like four
Speaker 3: times higher in people with PCOS compared to people without
Speaker 3: PCOS regardless of BMI. Huh, though that incidence does increase
Speaker 3: with increasing BMI.
Speaker 4: Okay.
Speaker 2: And so basically, the the outcome of this like domino
Speaker 2: like the path that the dominoes take. It might be different,
Speaker 2: just but we don't know why it might be different.
Speaker 2: But that's what results in these different phenotypes. But the
Speaker 2: end result for the most part is similar in terms
Speaker 2: of health consequences.
Speaker 3: I mean it is similar. It is not exact actually
Speaker 3: the same. It is similar, and then it's also like
Speaker 3: not exactly the same in terms of even those initial dominoes, right,
Speaker 3: because in some people we see this hyperandrogenism and in
Speaker 3: some we don't, but we still call it PCOS. Is
Speaker 3: that really the same disease or not? Is?
Speaker 4: Yeah? Is it?
Speaker 3: We don't know right now, We really don't know. We
Speaker 3: don't because we also don't know like what actually causes
Speaker 3: pcos R. Right. It's very strongly genetic. There is a
Speaker 3: big heritability component. It's like seventy percent heritable. Yeah, And
Speaker 3: that's not necessarily all strictly genetic. There's like at least
Speaker 3: twenty different gene losi in different populations. There's not one
Speaker 3: single gene, but there's also evidence of like epigenetic changes
Speaker 3: that we don't really know what is the trigger for
Speaker 3: these changes. But there's likely some epigenetic things that are
Speaker 3: involved in the like increased risk of PCOS, and then
Speaker 3: there's likely other environmental factors at play that we don't
Speaker 3: really understand. Right, what are all of these other triggers?
Speaker 2: I'm going to say it here because I didn't put
Speaker 2: any of this in my notes, but I didn't want
Speaker 2: to get into the evolutionary There are like a lot
Speaker 2: of different papers I read about the evolutionary origins of
Speaker 2: PCOS as proposed by certain researchers, and it is And
Speaker 2: I was like, ultimately, we don't understand what PCOS is,
Speaker 2: and so how can we really talk about what, like,
Speaker 2: how can we test these hypotheses if we don't know
Speaker 2: what it's caused by? And yeah, so that I didn't
Speaker 2: I don't have anything about that.
Speaker 4: I mean, yeah, because we don't.
Speaker 3: I feel like we don't even have a good We
Speaker 3: have a clinical definition, right, we can diagnostical definition, But
Speaker 3: are all are all of these phenotypes? Are all pcos
Speaker 3: the same?
Speaker 4: I don't know.
Speaker 3: We don't know, we don't know in terms of what
Speaker 3: we do about it and how we treat it. It
Speaker 3: really depends on what we're worried about, what the symptoms
Speaker 3: are that a patient or a person is worried about.
Speaker 3: Because because a lot of these symptoms of pcos are
Speaker 3: related to these androgenic hormones and related to this HPO axis,
Speaker 3: a lot of times we rely on birth control as
Speaker 3: one of the first line treatments for pcos, especially combination
Speaker 3: birth control like estrogen containing birth control, because what that
Speaker 3: does is it helps kind of override a lot of
Speaker 3: this HPO axis. It's going to negate any of these
Speaker 3: ovulatory dysfunctions, it's going to decrease your risk of undermetrial cancer.
Speaker 3: And the estrogen effect especially can help to alleviate a
Speaker 3: lot of the symptoms of excess androgens if those symptoms
Speaker 3: are unwanted, like acne and hersitism, because the estrogen what
Speaker 3: it does is it helps to address this decrease in
Speaker 3: sex hormone binding globulin, which then helps to decrease the
Speaker 3: amount of free testosterone that's circulating. Sometimes, though we might
Speaker 3: use anti androgen specific medications like sperona, lactone or other
Speaker 3: medicines if we're targeting some of those hyper andthrogen symptoms
Speaker 3: as a concern, but none of those are going to
Speaker 3: address the metabolic effects. Right, birth control is not going
Speaker 3: to change insulin resistance if that's present. By the way,
Speaker 3: we don't have a test for insulin resistance. There's no test.
Speaker 4: We don't have a test. We don't have a way
Speaker 4: to test for insulin resistance. Huh.
Speaker 3: We can test for risk of diabetes. But diabetes is
Speaker 3: not just insulin resistance. It's and it's we see our
Speaker 3: diabetes episodes. There's other ways that you can get diabetes
Speaker 3: besides just insulin resistance. But insulin resistance can lead to
Speaker 3: diabetes if you then have impaired glucose tolerance. But insulin
Speaker 3: resistance is like a first step if that's the pathway,
Speaker 3: and we can only see it if it's come to
Speaker 3: the point of, Okay, you have an increase in your
Speaker 3: A one C or you have an increase in your
Speaker 3: fasting glucose. But that's not directly a marker for insulin
Speaker 3: resistance itself, and we don't have a test for that.
Speaker 4: That's easy to do. I just I know that we did.
Speaker 2: Nope, we don't which explains why it's not part of
Speaker 2: the clinical picture exactly because you can't test for it.
Speaker 3: Can't test for it, right, you cannot test for it.
Speaker 3: So but if there is evidence, especially of like glucose intolerance, right,
Speaker 3: like increased ae C or something like that, then you
Speaker 3: can address that with met Foreman is usually the first line,
Speaker 3: and that's a drug that we use for diabetes. It
Speaker 3: helps to increase insulin sensitivity in our tissues. It sometimes
Speaker 3: can also cause weight loss, which may or may not
Speaker 3: be desired, depending on the situation. What's very very interesting
Speaker 3: about met Foreman is that it also has data that
Speaker 3: it helps to regulate ovulation and what exactly is the
Speaker 3: mechanism there, Like does that give us any insight.
Speaker 4: Into what is going on here?
Speaker 3: I don't know that it does, but I just still
Speaker 3: think it's so interesting.
Speaker 4: Right is there? Does that is that?
Speaker 2: Does that help shine a light on the link between
Speaker 2: I think process.
Speaker 3: It helps chin to light on there because when you
Speaker 3: look at these grap we should post one of these
Speaker 3: like graphs of what these feedback loops look like and
Speaker 3: how they're disrupted in pcos. There is a strong link
Speaker 3: between insulin resistance and hyperinsulinemia and and grogen production in
Speaker 3: the ovaries. So we know that that's like an inward arrow.
Speaker 4: There's just no.
Speaker 3: Backward arrow that that goes. Like, then why does the
Speaker 3: insulin resistance come up in the first place? That gods yees, yeah, yeah,
Speaker 3: Like is insulin resistance actually the primary mechanism? I don't know,
Speaker 3: But then why do we see Anyways, it's much but
Speaker 3: for people who maybe want to get pregnant on our
Speaker 3: struggle with infertility, sometimes met Forman can then be used
Speaker 3: to help alleviate the anovulation. It is not first line
Speaker 3: if the goal is pregnancy, though usually first line what
Speaker 3: we use as a medicine called letrozol or another similar
Speaker 3: medicine that triggers ovulation that's more directly triggering ovulate. But
Speaker 3: met Foreman can and it has good data that it
Speaker 3: can normalize ovulation to a regular degree, which can help
Speaker 3: with infertility if that's a goal. And then there's also
Speaker 3: an interest, of course in using newer medicines like glp
Speaker 3: ones which are the ozembics of the world, or other
Speaker 3: combination medicines. But we'll get there later in this episode.
Speaker 2: Arin quick question, give it to me menopause.
Speaker 3: Ah, yes, yeah, what's the question?
Speaker 2: Well, the question is, like I guess, the question is
Speaker 2: a very vague, unformed question. But just like for people
Speaker 2: who have PCOS, is their menopause experience any different?
Speaker 4: This is such a great question.
Speaker 2: No idea, Okay, no, no one has examined it.
Speaker 3: All of these papers are like, hey, yeah, so a
Speaker 3: lot of what we know about PCOS we think of
Speaker 3: as a reproductive disorder, and so its primary effects are
Speaker 3: in the reproductive years. So we don't have a lot
Speaker 3: of data on postmenopausal PCOS. Is the insulin resistance still
Speaker 3: a thing? Are you at higher risk for cardiovascular disease
Speaker 3: and type two diabetes postmenopausal compared to someone who has
Speaker 3: Like does your PCOS still exist postmenopause?
Speaker 2: Right, That's what I was trying to That's what I
Speaker 2: was trying to ask, and the great question, I guess.
Speaker 2: The other question then is Okay, So, and this maybe
Speaker 2: kind of gets into what I'm going to talk about
Speaker 2: a little bit, But like, you get a diagnosis of PCOS,
Speaker 2: you are not interested in becoming pregnant. You maybe are
Speaker 2: not interested in addressing any of the other symptoms of PCOS.
Speaker 2: Is there anything in your medical care. That is, like,
Speaker 2: we should have increased screening for cardiovascular disease. We had
Speaker 2: to have this in that.
Speaker 4: Is that something that physicians do do? Does anyone do it?
Speaker 4: Is the question I can't answer.
Speaker 3: That is the guidelines though that those are the guidelines,
Speaker 3: especially from the twenty twenty three update. You should be
Speaker 3: screened for potentially for sleep apnea, which not everyone is
Speaker 3: necessarily needs to be screened for sleep apnea, but if
Speaker 3: you have PCOS, you probably should at least be screened
Speaker 3: with like some of the questionnaires. You should be screened
Speaker 3: for diabetes, so checking in A and C. You should
Speaker 3: be screened for hyperlipidemia, even if you don't want to
Speaker 3: address any of the symptoms of hyperandrogenism. And it does
Speaker 3: not matter to you whether like you don't want to
Speaker 3: get pregnant, and so does it matter to you if
Speaker 3: you're not ovulating on a regular schedule. You do need
Speaker 3: to think about endometrial protection. You have to do something
Speaker 3: to reduce that risk of endometrial cancer. So that is
Speaker 3: something that you have to think about. And yeah, those
Speaker 3: are I mean, those are the main things. There's there's
Speaker 3: probably more than that. I'm forgetting off the top of
Speaker 3: my head. Also, depression and anxiety are higher in people
Speaker 3: with PCOS. Why we don't know is that just because
Speaker 3: of how people are treated with PCOS by the medical system,
Speaker 3: how long it can take to get a diagnosis, how
Speaker 3: much they're like ignored by the medical system.
Speaker 4: We don't know.
Speaker 3: Is it just because it does it actually have anything
Speaker 3: to do with PCOS and the like pathology there, or
Speaker 3: is it all.
Speaker 4: Just our medical system? We don't know.
Speaker 3: Yeah, but it's an important thing to keep in mind
Speaker 3: as well as Yes, society exactly, Aaron, that was only
Speaker 3: twice as long as I intepreated?
Speaker 4: So tell me how did we get to hear? What
Speaker 4: do we know?
Speaker 5: You know, those are some great questions. Let's let's get
Speaker 5: into it, Okay. For all that we still don't know
Speaker 5: about the biology of PCOS, this condition can teach us
Speaker 5: so much when it comes to the power of societal expectations,
Speaker 5: the inadequacy of a name, our failure to provide care
Speaker 5: to all who need it, and how silence, stigma, and
Speaker 5: shame can profoundly.
Speaker 2: Deepen the impact of a medical condition. At least it
Speaker 2: can teach us those things if we are willing to listen.
Speaker 4: Yeah, can we learn those things?
Speaker 2: Can we learn those things? Prevalence estimates of pcos vary.
Speaker 2: The most common numbers I've seen are six to twenty
Speaker 2: percent of people assigned female at birth. Others say, you know,
Speaker 2: one in ten, a huge, huge prevalence, and yet PCOS
Speaker 2: receives less funding for research compared to other similarly prevalent conditions.
Speaker 2: There is less awareness, both in the medical community as
Speaker 2: well as within the general public, and we still lag
Speaker 2: behind in terms of treatment options and medical knowledge about pcos. Clearly,
Speaker 2: not enough of us are listening. Hopefully that will change
Speaker 2: thanks to the incredible advocacy work by some groups and individuals,
Speaker 2: and thanks to the Internet, which I never thought i'd say,
Speaker 2: but truly thanks to the Internet where people with PCOS
Speaker 2: can find the support and community that is so often
Speaker 2: lacking in their everyday lives or in interactions with their
Speaker 2: healthcare provider. Before I go any further, I want to
Speaker 2: shout out one advocate in particular, and that is doctor
Speaker 2: Stacey L. Williams, a social health psychologist at East Tennessee
Speaker 2: State University and author of an incredible book that I
Speaker 2: read for this episode titled The Psychology of PCOS. Building
Speaker 2: the science and breaking the silence as someone who does
Speaker 2: not have PCOS but thought they knew a thing or
Speaker 2: two about it, which it turned out to be true
Speaker 2: in the literal sense. I found this book to be
Speaker 2: incredibly eye opening and perspective shifting truly, and almost everything
Speaker 2: that I'm going to talk about when it comes to
Speaker 2: PCOS today and some of the issues that we see
Speaker 2: comes from this wonderful book. But before we get into
Speaker 2: today in the today's landscape, let's go back in time
Speaker 2: to get a sense of the lengthy history of this condition.
Speaker 2: So PCOS is likely an ancient disease in humans, and
Speaker 2: it's probably not limited to our species. One of the
Speaker 2: challenges with understanding the root causes of PCOS is not
Speaker 2: having a naturally occurring animal model. But I did come
Speaker 2: across a paper that described Reese's monkeys that had naturally
Speaker 2: occurring high levels of testosterone and seem to exhibit some
Speaker 2: of the clinical picture of PCOS. It's still like, it's.
Speaker 4: Not clear, you know. Yeah.
Speaker 2: The first likely descriptions of the condition in humans come
Speaker 2: from ancient Greece in hippocrates Diseases of Women text written
Speaker 2: in the fourth century BCE.
Speaker 4: Oh gosh, can't wait for this quote.
Speaker 2: But those women whose menstruation is less than three days
Speaker 2: or is meager are robust, with a healthy complexion and
Speaker 2: a masculine appearance. Yet they are not concerned about bearing children,
Speaker 2: nor do they become pregnant.
Speaker 4: End quote. Okay, yep.
Speaker 2: Other ancient texts mention hersatism or hersaitism in combination with
Speaker 2: changes in mensis as a condition, and another Greek physician,
Speaker 2: Soreness of Ephesus, wrote around the second century CE quote
Speaker 2: sometimes it is also natural not to menstruate at all.
Speaker 2: It is natural too in persons whose bodies are of
Speaker 2: a masculine type. We observe that the majority of those
Speaker 2: not menstruating are rather robust, like mannish and sterile women.
Speaker 4: Quote.
Speaker 2: I know language is not great, ary, yeah, but what
Speaker 2: these descriptions show is that pcos was likely an ancient
Speaker 2: disorder and common enough that it was mentioned in several
Speaker 2: old medical texts, and that it has always been described
Speaker 2: as violating expectations of femininity. The next description that historians
Speaker 2: point out comes from seventeen twenty one, when an Italian
Speaker 2: physician Vallisneri described a married, quote unquote infertile woman who
Speaker 2: died young at twenty one years and upon autopsy was
Speaker 2: found to have shiny ovaries with a white surface, and
Speaker 2: the size of ovaries as pigeon eggs or ovaries the
Speaker 2: size of pigeon eggs.
Speaker 4: Okay, I have no idea, like how big a pigeon
Speaker 4: egg is. I'm not sure either. I should have imagined
Speaker 4: they're small, though, like pigeons aren't very big birds. Yeah, Okay, I.
Speaker 2: Don't know all right. Additional mentions of what was likely
Speaker 2: pcos popped up throughout the eighteenth and nineteenth centuries, including
Speaker 2: from Rokotanski, the famous pathologist I mentioned before on the
Speaker 2: podcast who did like tens of thousands of autopsies, and
Speaker 2: this period, especially in like the late nineteenth century early
Speaker 2: twentieth century, was crucial time for building a foundation of
Speaker 2: knowledge for understanding the role of different hormones in our
Speaker 2: physiology and what could happen when things do not go
Speaker 2: as expected. This was also when the testosterone equals male
Speaker 2: estrogen equals female false dichotomy was established.
Speaker 4: Oh love that? Yeah?
Speaker 2: Still on learning that.
Speaker 4: I think? Yeah.
Speaker 2: And so while that piece of the puzzle, like the
Speaker 2: hormone piece of the puzzle, wouldn't get slotted into pcos
Speaker 2: until the nineteen sixties, when researchers demonstrated the ovaries role
Speaker 2: in producing androgens. A complete clinical picture of the condition
Speaker 2: was formed by nineteen thirty five. Wow less complete.
Speaker 4: Yeah.
Speaker 2: That year, two physicians Irving Freilerstein and Michael Leo Leventhal
Speaker 2: published a paper titled AIM and Area associated with bilateral
Speaker 2: polycystic Ovaries.
Speaker 4: Okay, there you.
Speaker 2: Go, and in it they described the case reports that
Speaker 2: they had collected over the previous few years while investigating
Speaker 2: factors underlying difficulty getting pregnant. They followed these patients for
Speaker 2: long periods of time and truly got to know them,
Speaker 2: got to know their histories, got to know just everything
Speaker 2: about them. It was sort of this like, you know what,
Speaker 2: let's just cast a wide net and see what comes out.
Speaker 2: And by doing this, which is not a very common
Speaker 2: thing done today, they were able to draw out patterns
Speaker 2: that otherwise might have been missed. A subset of their
Speaker 2: patients had started menstruating years before, but their periods since
Speaker 2: had been unpredictable or just lacking entirely. They tended to
Speaker 2: have more hair growth than average and enlarged cystic ovaries,
Speaker 2: often larger than the uterus even at least a few,
Speaker 2: and they performed surgeries on a few of their patients
Speaker 2: to remove the cysts and part of the ovaries, both
Speaker 2: for diagnostic as well as therapeutic purposes, and a couple
Speaker 2: of people actually delivered children after the surgery. So what
Speaker 2: was different about Stein and Levenhal's clinical picture, like, why
Speaker 2: is this the one that put pcos on the medical map?
Speaker 4: So to speak?
Speaker 2: They were the first to describe the triad of polycystic
Speaker 2: ovarian morphology, hersitism, and infrequent irregular periods. And of course
Speaker 2: this is not a perfect clinical picture, which over the
Speaker 2: decades has evolved to account for more diverse symptoms and
Speaker 2: still maybe as one could describe it as incomplete lacking yes,
Speaker 2: and their focus on ovarian cysts, ultimately leading to the
Speaker 2: name polycystic ovary syndrome was misleading since cysts are not
Speaker 2: always present.
Speaker 3: Yeah, or like yeah, it's not quite accurate. Yeah, you
Speaker 3: could say, I mean, if you assist just a fluid
Speaker 3: filled thing, then sure, sure we'll call it. Sure, Yeah,
Speaker 3: that be presnent. Yeah, doesn't have to be present exactly.
Speaker 3: But what they did was provide a starting point and
Speaker 3: drive interest in this condition and in the decades since,
Speaker 3: researchers have added detail and depth to what we know
Speaker 3: about PCOS, from diagnosis to possible treatments, but not nearly enough.
Speaker 3: To quote doctor Stacy Williams, who's the author of the
Speaker 3: Psychology of PCOS, quote, it is unfathomable that in the
Speaker 3: twenty first century we are still grappling with diagnosis and
Speaker 3: treatment for PCOS. After more than eighty five years since
Speaker 3: PCOS was formally identified, doctors still lack knowledge of the syndrome.
Speaker 3: Combine that reality with a continued lack of cultural sensitivity
Speaker 3: of providers towards their patients, and we have a recipe
Speaker 3: for continued delays in diagnosis, biased interactions, and increased risk
Speaker 3: of worse health outcomes.
Speaker 4: End quote.
Speaker 2: Yeah, the resulting cost of this is huge on the
Speaker 2: economic side, eight billion dollars annually in the US alone,
Speaker 2: that was estimated in twenty twenty two. That's a split PCOS,
Speaker 2: and that's split about equally between reproductive issues and metabolic
Speaker 2: vascular issues, and is likely an underestimate. Aaron, you took
Speaker 2: us through some of the physical costs associated with PCOS,
Speaker 2: some of which can be substantial, but the psychological costs
Speaker 2: of this condition can be immeasurable and mostly go unacknowledged,
Speaker 2: at least in the medical literature. PCOS, like many chronic conditions,
Speaker 2: reveals a divide between how society expects you to act, look,
Speaker 2: and feel and how you actually act, look and feel.
Speaker 2: The price for not meeting those expectations can be steep,
Speaker 2: whether it results from medical gaslighting, bullying, or internalized stigma.
Speaker 2: People with PCOS are at a higher risk of depression
Speaker 2: and anxiety. Like you said, and it's difficult to disentangle
Speaker 2: whether these mental health impacts are a direct or indirect
Speaker 2: consequence of PCOS. Is it hormone dysregulation, is it the
Speaker 2: medications someone has prescribed? Is it the stigma you face
Speaker 2: with PCOS? Is it not just one thing but many.
Speaker 2: We don't have a good answer, but if we want
Speaker 2: to find one, what we need is more information, not
Speaker 2: just about the biological underpinnings of pcos, but especially the
Speaker 2: lived experiences. What is it like to live with a
Speaker 2: condition whose symptoms mark you visibly or invisibly as not
Speaker 2: conforming to societal norms or medical expectations. How does our
Speaker 2: society or our medical establishment treat someone with PCOS? And
Speaker 2: how is that wrapped up in ingrained notions of gender
Speaker 2: and sexuality. Let's get into it, okay, and I'm roughly
Speaker 2: breaking it down between outside of clinic and inside clinic.
Speaker 4: Okay.
Speaker 2: As you described, Aaron PCOS is associated with a broad
Speaker 2: array of signs and symptoms, some of which are visible,
Speaker 2: like you know what is called male pattern body hair
Speaker 2: or baldness, weight gain, others which aren't visible, such as
Speaker 2: irregular periods, difficulty getting pregnant, but many of which challenge
Speaker 2: gender norms. Our society has hammered into us that women
Speaker 2: should not be hairy, that in fact, any body hair
Speaker 2: or facial hair is shameful and disgusting, and we should
Speaker 2: take steps to conceal.
Speaker 4: It and avoid it. La away.
Speaker 2: I mean, bearded ladies were a staple of circuses for
Speaker 2: goodness sake. Our society equates fatness with a moral failing,
Speaker 2: believing that it demonstrates a lack of self control, and
Speaker 2: women especially should be delicate, slender angels. Our society tells
Speaker 2: us we become women when we get our first period,
Speaker 2: and that are flee bleeding is a powerful reminder of
Speaker 2: our womanhood. Oh God, sorry, nauseous. Our society assumes that
Speaker 2: every woman will want to give birth. Our society expects
Speaker 2: that every person assigned female at birth should look a
Speaker 2: certain way, act a certain way, and want certain things,
Speaker 2: and PCOS can throw a wrench into society's expectations sometimes
Speaker 2: because we are raised in the society and these expectations
Speaker 2: are deeply ingrained in us. This can lead to intense
Speaker 2: feelings of stigma that come from within if you don't
Speaker 2: menstrate regularly, and menstruation, though itself is stigmatized, is associated
Speaker 2: with womanhood. Does that mean that you are less of
Speaker 2: a woman? Of course not, but that is a difficult
Speaker 2: thing to unlearn. The author of the Psychology of PCOS
Speaker 2: interviewed fifty people with the condition for the book and
Speaker 2: included snippets of the interviews, which which we're so insightful, Like,
Speaker 2: I loved that approach so much. I think it's so important,
Speaker 2: and I want to share a few throughout the rest
Speaker 2: of this So Joe late twenties gender queer non binary
Speaker 2: described being bullied for having male pattern facial hair when
Speaker 2: they were younger and said that they quote spent a
Speaker 2: lot of time trying to get rid of my body hair,
Speaker 2: to the extent that nobody would even be able to
Speaker 2: know I even had it. So I feel that it's
Speaker 2: a cultural mandate for people who are trying to pass
Speaker 2: as women that you can't have even stubble in places
Speaker 2: that you're not supposed to have hair, which is pretty
Speaker 2: much everywhere except your head. It's a lot of time
Speaker 2: and a lot of paranoia to try and maintain that
Speaker 2: appearance if that's not what your body is actually doing.
Speaker 2: And that was a big source of feeling invalidated as
Speaker 2: a woman for a long time. End quote And like, Okay,
Speaker 2: I don't have PCOS as far as I know, but
Speaker 2: I do have a lot of body hair, thanks genetics,
Speaker 2: And it has been and continues to be a source
Speaker 2: of shame and like embarrassment and anxiety in my life.
Speaker 2: And it was just like it.
Speaker 4: Still to this day. Oh anyway, yes, no, it's very real.
Speaker 2: It's very real. And then there's another first hand account
Speaker 2: or another like snippet I want to share from Kim
Speaker 2: mid thirties cis gender, who said, quote before I was
Speaker 2: diagnosed with PCOS, I really just felt like my body
Speaker 2: was broken, and I think I had a lot of
Speaker 2: shame around not understanding why I was having trouble with
Speaker 2: periods and what this pain was that other people in
Speaker 2: my life, who menstraight don't have. So what was going
Speaker 2: on for me? Why was I weird? And I think
Speaker 2: that shame made me feel isolated because I couldn't talk
Speaker 2: about it or I didn't know I could talk about it.
Speaker 4: End quote.
Speaker 2: Stigma can also arise from other people. One person interviewed
Speaker 2: in the book describes getting facial hair shavers for Christmas
Speaker 2: from their mom. Oh yeah, I mean I bullied all
Speaker 2: throughout middle school and high school for body hair.
Speaker 4: Yeah. Why, Oh my gosh, why body hair?
Speaker 2: Like I mean that we could do a whole episode
Speaker 2: on that, but I think we should, Maybe we should.
Speaker 2: I think part of it too, is like Razor companies
Speaker 2: were like, oh, we're missing half the population.
Speaker 4: Yeah, yeah, you're disgusting. You're disgusting.
Speaker 2: Your hair is disgusting, it's unhealthy, it's unhygienic.
Speaker 4: Yeah, it makes me so upset.
Speaker 2: And then Meg early twenties cis gender, talks about a
Speaker 2: college field trip for her geography major involving canoeing.
Speaker 4: Quote.
Speaker 2: The professor was concerned about my ability to canoe because
Speaker 2: I'm overweight, Therefore I might not have enough stamina even
Speaker 2: though I've been kayaking all my life and I'm very
Speaker 2: good at canoeing and kayaking. Quote yeah, I mean that's
Speaker 2: Another person interviewed described how her parents don't really quote
Speaker 2: unquote believe in PCOS and that the weight is completely
Speaker 2: a matter of self control.
Speaker 4: The amount of fat shaming.
Speaker 2: It's it's ridiculous, yea, it's overwhelming. Yeah, yeah, yeah, yeah,
Speaker 2: there is. There is nothing inherently shameful about any part
Speaker 2: of PCOS. But because we are exposed to societal expectations
Speaker 2: from the minute we are born, and multiple symptoms of
Speaker 2: PCOS do not align with those expectations, stigma remains a
Speaker 2: huge issue, whether that comes from within or from without. Yeah,
Speaker 2: but not everyone experiences PCOS in the same way. So,
Speaker 2: for instance, some cisgender women may feel self conscious about
Speaker 2: their facial hair. Others may be done performing femininity by
Speaker 2: removing that hair, and they're like, no, I'm growing it
Speaker 2: out right, I don't care, it doesn't bother me. And
Speaker 2: other people that don't identify as women may welcome that
Speaker 2: facial hair, feeling that it more closely aligns with their
Speaker 2: gender identity. Along those lines, infrequent or unpredictable periods might
Speaker 2: be a painful reminder to cisgender women who are trying
Speaker 2: to become pregnant, or a source of anxiety for those
Speaker 2: who do not want to be pregnant, while absent periods
Speaker 2: might be the desired outcome for people who find them
Speaker 2: distressing since they do not align with their gender, and
Speaker 2: then there's everything in between. People can feel a million
Speaker 2: different ways about these different symptoms. Kendall late twenties non
Speaker 2: binary describes the mixed feelings that can arise quote, but
Speaker 2: the gender dysphoria. I feel like PCOS actually helps a
Speaker 2: little bit, but it also kind of makes it worse
Speaker 2: because I'm having all these problems that revolve around my
Speaker 2: female anatomy. So it's kind of like a push and
Speaker 2: pull of two differing emotions. And before I felt as
Speaker 2: though I was ready to identify as transgender, it definitely
Speaker 2: made me feel terrible about my body, very much like
Speaker 2: I was unlikable, unattractive to other people. But now I
Speaker 2: feel the oposit I feel like it makes me more
Speaker 2: attractive because I'm transgender now and I present masculinely, but
Speaker 2: at the same time, the health aspects and if I
Speaker 2: don't watch myself, I could gain weight. Then I will
Speaker 2: feel even worse about myself end quote. Yeah. There hasn't
Speaker 2: been very much research on gender identity and PCOS, but
Speaker 2: one study looking at the experience of transgender men with
Speaker 2: PCOS found less gender dysphoria and less negative body image
Speaker 2: in those with PCOS compared to those without interesting there
Speaker 2: is no hard and fast rule for how someone will
Speaker 2: experience PCOS. Maybe there's shame or stigma. Maybe there's confidence
Speaker 2: and power, Maybe there's discomfort or sadness. Maybe there's empathy
Speaker 2: and understanding, and maybe there's everything all at once or
Speaker 2: at different stages of your life. Each experience is unique
Speaker 2: and influenced by a person's inner and outer world. Do
Speaker 2: they have someone or a community of someone's that supports,
Speaker 2: understands and listen to them. Part of what perpetuates stigma
Speaker 2: in PCOS is a lack of awareness surrounding this condition.
Speaker 2: People don't know what it is, and since it affects
Speaker 2: those assigned female at birth, there's a tendency to assume
Speaker 2: that it's a gynecological disorder. And while we don't talk
Speaker 2: about anything down there, down there no limits, that's not
Speaker 2: the light company. Yeah, and this unwillingness to engage with
Speaker 2: PCOS because it's seen as a quote unquote women's disease,
Speaker 2: shrouds it in silence, leading to less understanding and less
Speaker 2: interest in both the general public as well as the
Speaker 2: medical community. Just as society has its expectations of what
Speaker 2: a woman should be, medicine has their own notion of
Speaker 2: what PCOS looks like and how it should be managed. Yeah,
Speaker 2: they do, and often this leads to a much narrower
Speaker 2: view of this condition that excludes people who might not
Speaker 2: fit the you know, quote unquote typical clinical picture.
Speaker 4: R which is phenotype A and B or classic PCOS yep, yep.
Speaker 2: And this results in delays and diagnosis and inappropriate treatment.
Speaker 2: Because of its impact on fertility, PCOS is often seen
Speaker 2: primarily as a condition of heterosexual women who are struggling
Speaker 2: to become pregnant, and treatment is prescribed accordingly.
Speaker 4: Yep.
Speaker 2: This erases the experience of so many people who do
Speaker 2: not fit that description. M hm, oh, you've got irregular periods.
Speaker 2: Let's get you on some birth control so you'll bleed monthly,
Speaker 2: which doesn't take into consideration that someone might not want
Speaker 2: to have periods at all.
Speaker 3: Yeah, maybe sorry, Just like this is my personal opinion, like,
Speaker 3: why would we want to have periods?
Speaker 4: Why? Why?
Speaker 3: Right?
Speaker 4: Some people do? People do? People definitely don't. Uh huh. Absolutely,
Speaker 4: people feel different ways about this. There's no one way.
Speaker 5: Yeah, or maybe your doctor says it's you know that
Speaker 5: facial hair, it's from your hormone imbalance.
Speaker 2: You're a good candidate for electrolysis. Let's set up an
Speaker 2: appointment for you. Again, pointing out ways that you don't
Speaker 2: conform to gender expectations and pressuring you into performing femininity
Speaker 2: and making you feel othered and rejected, whether or not
Speaker 2: it's well intentioned. And then there's you really need to
Speaker 2: try harder to lose weight. It's not healthy. Are you
Speaker 2: exercising at all? You should eat less processed foods.
Speaker 4: You're doing it to yourself.
Speaker 2: You're doing it to yourself. Assuming that someone's weight is
Speaker 2: solely due to poor diet or poor health behaviors not
Speaker 2: related to PCOS, and that's someone's weight is entirely responsible
Speaker 2: for all their symptoms. Oh, you have pain, you should
Speaker 2: try to lose some weight.
Speaker 3: Also, assuming that their weight is the problem at all. Yes, yeah,
Speaker 3: but assuming that their weight, that their BMI is a problem,
Speaker 3: because obesity is a quote unquote disease like oh, it drives.
Speaker 2: Me, and this weight bias in medicine can lead to
Speaker 2: disordered eating, or maybe the doctor will say something like, okay,
Speaker 2: you're sure you don't want to become pregnant, Well, then
Speaker 2: there's not really anything you need to worry about.
Speaker 4: Oh gosh, that one gives me palpitations.
Speaker 2: One hundred percent. And this is you know, as you described,
Speaker 2: PCOS is associated with other health outcomes not related to fertility, right, diabetes,
Speaker 2: cardiovascular disease, high cholesterol, high blood pressure, fatty liver disease,
Speaker 2: and a mutual cancer metabolic syndrome.
Speaker 5: I mean there's like, yeah, sleep apnia, sleep apnia.
Speaker 4: Yeah.
Speaker 2: The author of the psychology of PCOS, who has the
Speaker 2: condition herself, said that in the thirty years since her diagnosis,
Speaker 2: no doctor has ever told her about these other health consequences.
Speaker 2: And I get, you know, n of one anecdote, but
Speaker 2: still that is not a unique experience.
Speaker 3: Well, and I just have to say this is where
Speaker 3: like I honestly was, so I'm a primary care provider, Yeah,
Speaker 3: I care for people with PCOS all the time. I
Speaker 3: was so embarrassed by how little I knew about the
Speaker 3: extent of the metabolic complications and how important they are
Speaker 3: first of all, regardless of BMI. Second of all, like
Speaker 3: to at least screen for despite how flawed our screening
Speaker 3: tools might be, and in everyone like it. Just it
Speaker 3: is not as well known as it should be, despite
Speaker 3: efforts to standardize these guidelines and get this information out there,
Speaker 3: and despite the fact that it is much better today
Speaker 3: than it was like prior to twenty eighteen.
Speaker 2: Yeah, I mean, that's it's very true. And I have
Speaker 2: a study that was reported on It was back in
Speaker 2: two thousand and seven, so prior to twenty eighteen, but
Speaker 2: it was testing US medical residence knowledge of pcos who
Speaker 2: I bet it was bad.
Speaker 4: Oh.
Speaker 2: They found that they scored on average fifty percent and
Speaker 2: that only a subset scored higher than seventy percent, like
Speaker 2: who were specializing in women's health. I think, Okay, yeah,
Speaker 2: huh huh. That is abysmal for a condition that affects
Speaker 2: one intent ten people conservatively assigned female at birth. It's inexcusable.
Speaker 2: And that's also an underestimate, right, Like one estimate I
Speaker 2: saw suggested that seventy percent of cases go undiagnosed. Wow
Speaker 2: wa yeah yeah, if you don't fit the classical clinical
Speaker 2: picture phoenotype A and B. Your doctor might dismiss you.
Speaker 2: They'll point out your weight and say, ah, but you're
Speaker 2: not obese. I don't think it's PCOS. You're thin or
Speaker 2: while you're older, maybe your periods are just slowing down
Speaker 2: even if they've been quote unquote slow your whole life.
Speaker 2: Delays and diagnosis for PCOS are exacerbated by race, by
Speaker 2: socioeconomic status, and by gender identity. The term women's health,
Speaker 2: along with all the other gendered language surrounding PCOS, illustrates this.
Speaker 2: But of course this doesn't apply to all healthcare providers,
Speaker 2: and some people have really great experiences with their individual providers,
Speaker 2: But even for them, even for those providers and overall,
Speaker 2: lack of knowledge about PCOS is limiting. What might the
Speaker 2: trans non binary experience be like for someone with PCOS?
Speaker 2: What do we know about hormone replacement therapy and PCOS?
Speaker 2: Is a healthcare provider equipped to answer those questions or
Speaker 2: willing to look for the answers? Do the answers even exist?
Speaker 2: There needs to be a shift in the way that
Speaker 2: we diagnose, treat, study, and talk about PCOS. We need
Speaker 2: to incorporate mental health care do a better job educating
Speaker 2: healthcare providers, raise awareness with the general public, improve treatment options,
Speaker 2: conduct more research into every aspect of this, and have
Speaker 2: more compassion and self compassion. Unfortunately, these changes won't happen overnight,
Speaker 2: but progress is being made by advocacy groups, by online
Speaker 2: communities where people can learn and share, and by some
Speaker 2: researchers who are trying to better understand this condition. And so,
Speaker 2: speaking of which, I'll turn it over to you, Aaron,
Speaker 2: to tell us where we stand today when it comes
Speaker 2: to PCOS.
Speaker 4: I can't wait. I have a huge surprise for you erin.
Speaker 3: Oh, okay, I'm going to take this whole thing in
Speaker 3: these last ten minutes and turn it on its head
Speaker 3: and then drop the mic and walk away.
Speaker 4: Ready, okay, yes, please, you said already.
Speaker 3: Most papers cite an estimated prevalence anywhere between five or
Speaker 3: six and twenty percent. Most of the newer papers, like
Speaker 3: the newest twenty twenty three guidelines said maybe ten to
Speaker 3: thirteen percent. Okay, but know the prevalence is thought to
Speaker 3: be relatively homogeneous across the globe, with maybe slightly higher
Speaker 3: prevalence in people of Southeast Asian descent and Eastern Mediterranean descent.
Speaker 4: Underlying that we don't know.
Speaker 3: And there's maybe some data that it's increasing in the
Speaker 3: recent decades, but it's very unclear to me whether this
Speaker 3: is related to any true increases in incidents or just
Speaker 3: increasing awareness and diagnosis or things like that. So when
Speaker 3: it comes to current research, you laid it out for
Speaker 3: us really nicely. Arin, there's a lot to be desired
Speaker 3: for me. I kind of just was like, what do
Speaker 3: I want to know about pcls. We know how much
Speaker 3: insulin resistance is a major factor, but we don't have
Speaker 3: any essays that can really measure insulin resistance, so love,
Speaker 3: I'd love more research on that, and there's certainly people
Speaker 3: doing that, and there are ways to measure it, it's
Speaker 3: just that they're not easy to do Clinically, They're like
Speaker 3: time intensive, labor intensive, expensive, so they can't be used.
Speaker 3: So then people are trying to come up with like, Okay,
Speaker 3: what is something that we can use that like measures
Speaker 3: up to these gold standard versions. There's also a lot
Speaker 3: of work that needs to be done that is being
Speaker 3: done on like understanding some of this kind of higher
Speaker 3: level what is this underlying cause, what is linking insulin
Speaker 3: resistance and this hyperandrogenism. Are these kiss peptins and other
Speaker 3: like peptides and receptors in our brain, in our hypothalamus
Speaker 3: Are those involved? Do we have a master regulator switch
Speaker 3: that we can find that we could target. We don't know,
Speaker 3: but a lot of people are working on potentially looking
Speaker 3: at other targets for medications. I mentioned glps. These are
Speaker 3: all the rage right now. GLP one receptor agonists. We
Speaker 3: need to do an episode on these they I know
Speaker 3: they What would they would be target is in part
Speaker 3: this insulin resistance because what they helped do is kind
Speaker 3: of regulate insulin release from our pancreas. And so there
Speaker 3: was a study that came out recently that looked at
Speaker 3: GLP ones alone plus really interesting combinations of glps plus
Speaker 3: other medicines including estrogen for pcos and they found that
Speaker 3: in some at least in this study which was on
Speaker 3: mice and rats, I actually don't remember if it was
Speaker 3: mice or rats, but they found a better treatment like
Speaker 3: alleviation of all of the various things that they look
Speaker 3: at in mice and rats with pcos then compared to
Speaker 3: met foreman, which is very interesting. The GLP plus estrogen combination.
Speaker 2: Yeah, the effects are so broad, so broad, it's really fascinating,
Speaker 2: and it goes like way beyond. It's like, you know,
Speaker 2: weight loss from GLP ones versus weight loss from not
Speaker 2: golp ones, and it's like there are extra effects. Yeah,
Speaker 2: Like it's just like what's happening.
Speaker 3: Well, And like the cardio the cardiologists are on the
Speaker 3: cardiovasca effects are so good, the Kid's protection, the and.
Speaker 2: Care episode on jlp ones and cardiovascular disease and heart
Speaker 2: failure especially, so if you are interested.
Speaker 3: Check out it's it's pretty major. They're also still very expensive,
Speaker 3: and any new drugs that have come out were going
Speaker 3: to be even more expensive, so that's another thing too. No,
Speaker 3: but here's where I want to take this whole table
Speaker 3: and flip it over. Ready for this, we have talked
Speaker 3: so far exclusively about PCOS polycystic ovarian morphology as a
Speaker 3: disease of people assigned female at birth, as in people
Speaker 3: with ovaries. However, polycystic ovarian morphology is not necessary to
Speaker 3: the definition right and in fact, the presence of ovaries
Speaker 3: themselves may not be in the metabolic phenotype of PCOS.
Speaker 3: That's a quote from one of the papers. Because we
Speaker 3: see very similar metabolic abnormalities and very similar hormonal disruptions
Speaker 3: in terms of free testosterone DGS, sex hormone binding globulin.
Speaker 3: Looking at all of these hormones in both people assigned
Speaker 3: female at birth with ovaries and in people with testicles.
Speaker 3: All right, so, huh, what's happening? What's happening? Aaron, I
Speaker 3: dug deep into this. I'm glad because there is a
Speaker 3: male equivalent that likely exists. However, it does not have
Speaker 3: a clinical definition, It does not have any clinical criteria.
Speaker 3: There are plenty of papers on it. Let's get into it. Yeah,
Speaker 3: we see in family members like male family members of
Speaker 3: people with PCOS, either siblings of or children of people
Speaker 3: with PCOS, in incidence in things like early onset androgenic
Speaker 3: alopecia so male pattern hair loss before age thirty five.
Speaker 3: We also see increases in metabolic syndromes including insulin resistance,
Speaker 3: type two diabetes, dyslipidymia, hypertension, cardiovascular disease, And in studies
Speaker 3: that have actually looked at this, we see a similar
Speaker 3: androgenic hormone profile. We can see increases in things like dhgas.
Speaker 3: We can see increases in antimulearian hormone males also make
Speaker 3: it and LH and FSH, and sometimes we see it.
Speaker 3: Sometimes we see a decrease in free testosterone, but then
Speaker 3: an increase in these other types of testosterones and things.
Speaker 3: So anyways, it is hypothesized based on all of this
Speaker 3: that first of all, there is in fact a similar
Speaker 3: metabolic and hormonal profile that is essentially a male equivalent
Speaker 3: a person with testes equivalent to PCOS, and that early
Speaker 3: onset male pattern hair loss is possibly one like physical
Speaker 3: visual marker for this syndrome. Except that about thirty percent
Speaker 3: of people assigned MAIL at birth have early onset androgenic alopecia.
Speaker 3: So does that mean that it's just not as specific
Speaker 3: as a marker. Does it mean that the incidence is higher?
Speaker 3: What does that mean we don't have multiple.
Speaker 2: Causes of it that exactly are not related to this syndrome.
Speaker 3: Yeah, And when we look at like the actual gen
Speaker 3: lo side that we know are associated with PCOS, we
Speaker 3: see those gene lo sie in these males that have
Speaker 3: these other symptoms. And yet when I, for example, when
Speaker 3: on up to date, which is where I often go
Speaker 3: as a clinician, but also when I'm like, does this
Speaker 3: and did I just miss this. It is nowhere mentioned
Speaker 3: on the PCOS page when I tried to look up
Speaker 3: like male equivalent.
Speaker 4: PCOS, it does.
Speaker 3: It's not a thing AARON because we don't have any
Speaker 3: test for it.
Speaker 2: Or presumably very many treatments. If somebody wants treat it
Speaker 2: would be.
Speaker 3: The same things in terms of like the metabolic symptoms, right,
Speaker 3: so we'd be talking about we'd be talking about met foreman,
Speaker 3: we'd be talking about and these other things. What would
Speaker 3: we need to do to treat the male pattern hair loss?
Speaker 3: Maybe we do the same kinds of things that we
Speaker 3: would do in females.
Speaker 4: But yeah, we don't have AARON. We don't. We do not.
Speaker 3: This is not recognized as a clinical condition. I want
Speaker 3: to make that very clear. But it is recognized in
Speaker 3: the literature dating back a couple decades, huh, at least
Speaker 3: a decade. And I feel like this highlights so PCOS
Speaker 3: for me, like the biggest takeaways that I have from PCOS,
Speaker 3: aside from just like how much we don't know, is,
Speaker 3: first of all, how much what we think of as
Speaker 3: binaries in medicine are spectrums, right, And where we put
Speaker 3: our cutoff markers, what is abnormally high testosterone for a female,
Speaker 3: what is abnormally low free testosterone for a male? All
Speaker 3: of this is somewhat arbitrary, right, and we've known this
Speaker 3: for a long time, but it becomes so much more
Speaker 3: important when we're looking at a condition like PCOS.
Speaker 2: Right, I find it very interesting, like this is I
Speaker 2: think that, yes, this is very revealing of the way
Speaker 2: that medicine considers bodies and binaries. And I'm just like
Speaker 2: thinking about this, like the male version of PCOS. What
Speaker 2: does that like? That should be able to tell us
Speaker 2: more about the root cause.
Speaker 3: It should, right, it should if we started looking at
Speaker 3: we started looking at why aren't we looking at it?
Speaker 4: I mean, there are people who are right because these
Speaker 4: papers exist.
Speaker 2: I know that you said that this is this is
Speaker 2: two decades old, or people start looking at you.
Speaker 3: It's more than ten years old. So two decades might
Speaker 3: have been an exaggeration.
Speaker 4: I don't remember when the first paper.
Speaker 2: Was because I feel like in this case, then the
Speaker 2: thing that really struck me about PCOS is that we
Speaker 2: are failing to capture people. We are failing to meet
Speaker 2: the needs that they have in many different ways. Sometimes
Speaker 2: that means we're not giving them the treatments that they want.
Speaker 2: We're not diagnosing them. Sometimes it means that we are
Speaker 2: giving them treatments they don't want, right, and that, oh,
Speaker 2: the birth control actually worsens your symptoms of anxiety and depression.
Speaker 2: And also I don't want periods, so I don't need
Speaker 2: to bleed monthly. But we also it's just like it
Speaker 2: shows our narrow view of this and how difficult it
Speaker 2: is to change these to change these perspectives and to
Speaker 2: like broad and actually broaden a clinical picture of something.
Speaker 3: It also, for me, highlights how stigmatized women's health is
Speaker 3: one percent because if you label a disease polycystic ovarian syndrome,
Speaker 3: inherently you assume it only affects people with ovaries, which
Speaker 3: means that we're ignoring it, we're dismissing it, we're not
Speaker 3: funding its research, which means that everyone's health is compromised
Speaker 3: because women's health affects men's health too.
Speaker 2: Women's health is health, it's human.
Speaker 3: It is human health, okay, And whether you have ovaries
Speaker 3: or whether you have testes, we should be looking at this.
Speaker 4: That's like my big rant.
Speaker 2: I feel like I have learned so so much huh
Speaker 2: about everything I know medicine about PCOS, but also about
Speaker 2: medicine and society and perspectives.
Speaker 3: And yeah, I know, and it just yeah, there's so much,
Speaker 3: there's so much still that we don't know. Yeah, especially
Speaker 3: like you were saying about the long term potential for
Speaker 3: complications postmenopausal PCOS PCOS intestines. You can't call it PCs.
Speaker 3: There's a paper that isn't yet published. Actually it's printed
Speaker 3: as a preprint, so presumably it will be published soon,
Speaker 3: but I do have a link to it. That's about
Speaker 3: how we need to rename PCOS because it's such a
Speaker 3: false name, like it's such a misnomer, and so we'll
Speaker 3: see what changes. Maybe it will change soon. What will
Speaker 3: we call it?
Speaker 4: I don't know.
Speaker 2: Someone was like this, I feel like I read something somewhere,
Speaker 2: and I wish I had kept the quote in, But
Speaker 2: it was like, this name is so ingrained in medicine
Speaker 2: that it's going to be as easy to change the
Speaker 2: name and get people to accept it as it is
Speaker 2: to find the ultimate cause which will then force a
Speaker 2: name rechanging or something like that, our name change.
Speaker 4: Yeah, I know.
Speaker 3: Yeah, Well, if you want to read so much more,
Speaker 3: so much, we can tell you so much about it
Speaker 3: or where to find it rather on our website.
Speaker 2: Yep okay I once again the book The secon Cology
Speaker 2: of PCOS by doctor Stacy Williams. Great book, check it out.
Speaker 2: And then for like the overall history kind of part
Speaker 2: of it, there was a paper I have a few,
Speaker 2: but there was a paper by Aziz and Adashi from
Speaker 2: twenty sixteen called Stein eleventhal eighty years on.
Speaker 3: I've got links to both the twenty twenty three and
Speaker 3: the twenty eighteen guidelines on the recommendations like evidence based
Speaker 3: Recommendations for Assessment and management, so those are both. There
Speaker 3: two papers that I loved that were just overviews of PCOS.
Speaker 3: One was from the Lancet Diabetes and Endocrinology from twenty
Speaker 3: twenty two, just titled Polycystical Variant Syndrome. And the other
Speaker 3: one is from BMJ Medicine from twenty twenty three titled
Speaker 3: polycystico very Syndrome, Pathophysiology and Therapeutic Opportunities. And then those
Speaker 3: couple of papers that I loved about the male equivalent
Speaker 3: of PCOS. One was titled Male Equivalent polycystico Variant Syndrome Hormonal,
Speaker 3: Metabolic and Clinical Aspects, and that was by Diguardo all
Speaker 3: from twenty twenty, and there's another one too from twenty eighteen.
Speaker 3: So you can find the list of sources from this
Speaker 3: episode and all of our episodes on our website, this
Speaker 3: podcast wikill you dot com under the episode stap yep.
Speaker 2: You can thank you again to Logan for providing the
Speaker 2: first hand account. We cannot, we don't have the words
Speaker 2: to thank you, but it means so much. Thank you,
Speaker 2: Thank you, it does.
Speaker 4: Thank you so much.
Speaker 2: Thank you to Bloodmobile for providing the music for this
Speaker 2: episode and all of our episodes.
Speaker 3: Thank you to Leanna and Tom and Brent and Pete
Speaker 3: and Mike and Jess and everyone else that's exactly right
Speaker 3: for making all of this possible.
Speaker 2: Yes, thank you, and thank you to you listeners. We
Speaker 2: hope that you also learned something from this or I
Speaker 2: don't know, Yeah, tell us what you think if you
Speaker 2: knew all of this already. Wow, yeah, that's impressive. Teach
Speaker 2: us something please, and thank you as always to our patrons.
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Speaker 2: Thank you well. Until next time, wash your hands
Speaker 4: You filthy animals.