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Identifying and supporting the lean PCOS patient with Lisa Costa-Bir and Sandra Villella

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Identifying and supporting the lean PCOS patient with Lisa Costa-Bir and Sandra Villella

Naturopath and herbalist Sandra Villella and fx Medicine ambassador Lisa Costa-Bir explore the case of the lean polycystic ovarian syndrome (PCOS) patient.

Sandra shares her clinical expertise in the management of the lean PCOS patient, offering insights into the differences between the classic PCOS phenotype.

Join the two naturopaths as they discuss differential diagnoses, signs and symptoms, comorbidities, and risk factors as well as relevant pathology testing to provide patients with an individualised, targeted treatment plan using nutritionals, herbs, and dietary interventions.

Full of clinical pearls, this episode is for practitioners looking to better identify the PCOS patient and broaden their understanding of this complex condition.

Covered in this episode

(00:26) Welcoming Sandra Villella
(01:26) Pathophysiology of PCOS and the lean verse classic PCOS Phenotype
(08:05) PCOS Diagnostic criteria in lean verse classic PCOS Phenotypes
(11:43) Androgens and blood testing
(13:28) Symptoms in lean verse classic PCOS Phenotypes
(15:55) Comorbidities in PCOS
(22:03) Dietary recommendations for lean PCOS women
(29:36) PCOS treatment aims and nutritional and herbal supplementation
(43:18) Thanking Sandra and final remarks

Key takeaways

  • PCOS is the most common endocrine disorder affecting females during their reproductive age.
  • 80% of women have the classical PCOS phenotype: overweight, insulin resistant, receding hairline.
  • The lean PCOS phenotype is described as the woman who isn't overweight or obese, and may have a relatively nutritious diet, but still has PCOS.
  • While obesity exacerbates insulin resistance, insulin resistance can exist in isolation.
  • Androgens are the core drivers of PCOS for both lean and classical phenotypes.
  • The most acceptable diagnostic criteria is the Rotterdam criteria.
  • Additional diagnostic criteria include clinical and/or biochemical hyperandrogenism: acne or hirsute presentation.
  • PCOS increases the risk of progression to gestational diabetes or type 2 diabetes, and cardiovascular conditions.
  • Dietary recommendations for the lean PCOS patient include: the inclusion of protein with every meal while incorporating low GI carbohydrates to ensure the maintenance of weight.
  • Apple cider vinegar balances blood sugar and improves insulin sensitivity.
  • Myo-inositol promotes glucose uptake and plays a role in insulin signalling transduction.
  • Peony and licorice help to reduce testosterone and manage cycle regularity.
  • Bitters, such as herbs containing berberine, help with glycaemic control.
  • Adaptogens for the management of stress.
  • Saw palmetto for female pattern hair loss.

Resources discussed and further reading

Sandra Villella

Sandra's website

Polycystic Ovarian Syndrome

Research: International Evidence-based Guideline for the assessment and management of polycystic ovary syndrome 2023
Article: Clinical summary and translation resources from the International Evidence-based Guideline for the Assessment and Management of Polycystic Ovary Syndrome 
Article: PCOS and nutritional approaches: Differences between lean and obese phenotype
Article: Meta-analysis of gene expression profiles of lean and obese PCOS to identify differentially regulated pathways and risk of comorbidities
Journal: Body Composition, Metabolic Characteristics, and Insulin Resistance in Obese and Nonobese Women with Polycystic Ovary Syndrome
Article: Influence of Subclinical Hypothyroidism on Women With Polycystic Ovary Syndrome: A Literature Review 
Article: The effects of flaxseed or its oil supplementations on polycystic ovary syndrome: A systematic review of clinical trials 
Article: ART outcomes in lean compared to obese phenotypes of polycystic ovarian syndrome

Fatty Liver Disease

Article: A multisociety Delphi consensus statement on new fatty liver disease nomenclature
Resource: New NAFLD Nomenclature
Research: Predictivity of fatty liver index for non-alcoholic fatty liver disease in lean females with polycystic ovary syndrome 


Lisa: Hi, and welcome to fx Medicine, where we bring you the latest in evidence-based, integrative, functional, and complementary medicine. fx Medicine acknowledges the traditional custodians of country. Throughout Australia, where we live and work, and their connections to land, sea, and community, we pay our respect to their elders past and present, and extend that respect to all Aboriginal and Torres Strait Islander peoples today. Joining us again is naturopath Sandra Villella. Sandra has been in clinical practice for almost three decades in Melbourne. She has a particular interest in women's health and is also a consultant, naturopath, and clinical leader for Jean Hailes, Australia's leading women's health organisation, a position she has held since 1999. Sandra also finds time to lecture at Torrens University, where she mentors final-year naturopathy students. Welcome to fx Medicine, Sandra. Thanks so much for joining us again.

Sandra: It's a pleasure. Thank you, Lisa.

Lisa: Excellent. Okay. So, I'm going to get straight into it. We learned so much from you last time you were on, and I wanted to chat with you again, but this time about polycystic ovarian syndrome, PCOS. Now, PCOS we know is incredibly common. In fact, it is the most common endocrine disorder affecting females during their reproductive age. And it's estimated that in Australia, 8% to 13% of females have PCOS. But really interestingly, this number increases to 20% in indigenous women, so about 1 in 5, which is huge. So, 80% of women have that classical PCOS phenotype that most of the prac is listening to would be familiar with.

And that's a client that's overweight, insulin resistant, hairline may be receding, but then they're getting hair in places they don't really want like their chin, their top lip, but less discussed is the lean PCOS phenotype, which is actually on the rise. And when we talk about lean PCOS, we're talking about the woman who isn't overweight or obese, and may have a relatively nutritious diet, but still has PCOS. So, let's explore this a little bit further. So, can you start, Sandra, by telling us a little bit about what's going on hormonally, what's going on in terms of that underlying pathophysiology in PCOS women who have that lean phenotype versus the classical?

Sandra: Yes. Okay. So, it is important to recognise that there is similarities between the overweight and normal weight PCOS patients. While obesity exacerbates the insulin resistance, the insulin resistance can exist in isolation. So, I'm introducing this insulin resistance because this is a key part of PCOS. So, what's interesting, and I want to start this right from the beginning because I think you know how much I go on about patients always, and practitioners always wanting to do estrogen clearance and thinking this is an estrogen dominant condition. I don't talk about estrogen dominance. Interestingly, this is absolutely not an estrogen dominance. And in fact, what could happen is there might be an unopposed estrogen, which I'll talk about later on, but essentially in females or those assigned female at birth, estrogen is the least important hormone here. And it's about androgens, which is like our third female hormones and insulin. So, if you think about those, they're the core drivers of this syndrome.

We need to start right from the beginning where PCOS, Polycystic Ovarian Syndrome, is actually a misnomer. They're not cysts. These are follicles. These are like follicles that it's like failed ovulation. All these attempts of good ovulation, you've got these failed follicles. And so it's really should be called follicular syndrome. And in fact, you know, you can have this syndrome and not actually have polycystic ovaries on ultrasound.

So, really, what kind of happens is, I think, when we think about the etiology of what causes PCOS, you know, it is largely unknown, but we do know that some of the factors, genetic factors, and basically, genetic factors and lifestyle have an impact. There's also this idea that in utero hormonal exposure has an impact. And then obesity has an impact.

So what actually happens in PCOS is that normally we've got one follicle that matures and undergoes ovulation. There's a pool of these, what we call primordial follicles that are there right from when we were born. And we have them when we are in utero. And usually, this selection of that follicle and for it to ovulate is strictly controlled, and strictly controlled so we can maintain our ovarian reserve and ensure our fertility is intact. And so what happens with PCOS is, the anti-müllerian hormone, which is in charge of "Come forward, please. Come forward, please, follicle, and ovulate." There's an imbalance between that and follicle-stimulating hormone. And it causes a halt of these follicular growth. And so what ends up happening is you have this characteristic pattern of lots of large numbers of primordial follicles growing and undergoing... They die. They cellular arrest. So, can you kind of visualise that and what's happening here?

Lisa: I can. It's so sad. They're dying little follicles.

Sandra: Yeah, yeah, yeah.

Lisa: Yeah. So, we're seeing this FSH, follicle-stimulating hormone that's not really doing what we want it to do. It's not stimulating...

Sandra: That's right.

Lisa: ...the follicles. And then we're seeing these high levels of insulin, high levels of androgens. We're not even going to worry about the estrogen because we know that that's not really a big part here. And then we see the AMH, anti-müllerian hormone is elevated. Tell me a little bit more about that LH, the luteinizing hormone.

Sandra: Yes. So, there is high levels of luteinizing hormone. And previously that used to be like a characteristic sort of diagnostic criteria, you know, high luteinizing hormone, low follicle-stimulating hormone. And so the luteinizing hormones are required for the androgen synthesis from these ovarian theca cells. So, theca cells are an important part and it comes from the Latin word of casing or the sheath. And so they need these high levels of luteinizing hormone combined with the low levels of FSH, and the decreased estradiol synthesis, because you see what happens is, normally the androgens are aromatised and cause estradiol, you know, cause estrogen that production. But the high LH and the low FSH and the subsequent decreased estradiol because of the aromatase kind of not being working, it results in anovulation. And there's not this dominant follicle that happens.

Lisa: And so this is obviously the same thing that is happening in classic, right? This lean PCOS.

Sandra: It is. It is.

Lisa: Underlying pathophysiology.

Sandra: Absolutely.

Lisa: We're seeing the same thing as the classical.

Sandra: Same thing. It's just that you've got one less thing to work with. And normally, you know, the primary intervention with overweight PCOS patients is a 5% to 10% loss of weight.

Lisa: Exactly.

Sandra: It actually addresses all the metabolic factors. It addresses all the reproductive parameters. And they usually will reinstate ovulation. Here, you don't want these patients to lose weight.

Lisa: Exactly.

Sandra: You have to address the insulin resistance. But you don't do that by weight loss. We use all the other tools that we have to make this insulin work better and address this dysglycemia, which seems to be very similar in both of these phenotypes.

Lisa: Interesting. So, can you tell us more about the diagnostic criteria for PCOS and what constitutes a diagnosis of that lean PCOS versus the classical? Because I know there's a few different criteria out there and I often think that I have a lot of patients coming to see me that PCOS maybe is misdiagnosed or even, dare I say, over diagnosed sometimes?

Sandra: Yes. Yes. And we will be sometimes, the ones who will question the diagnosis or indeed make the diagnosis. So, the most acceptable diagnostic criteria now is the Rotterdam criteria. You can have oligo or anovulation. So, typically in PCOS, it's oligomenorrhea rather than amenorrhea completely. So, these are the two people that are coming in who are having a period every 35, 40, 50 days. And this might be the first thing to alert you when you're seeing someone who comes in who's lean, who's having irregular periods, and you might be thinking, "Oh, they're an over-exerciser," or, "Oh, it's functional, hypothalamic amenorrhea." But you've got to be thinking, could it be polycystic ovarian syndrome? So, that one you don't need tests for, it's just health and you're having a period.

Lisa: Yeah.

Sandra: The other criteria is clinical and/or biochemical hyperandrogenism. That means the patient in front of you has got acne or they are hirsute and you need to ask because they might be really onto waxing and laser and may not show that, or biochemical hyperandrogenism. So, that means in their blood tests high androgens. It is not unusual to have a very hirsute person in front of you or with acne who has normal androgens in a blood test. And then the understanding is there's an increased sensitivity of the androgens at the level of the pilosebaceous unit, which is causing the acne or the hair follicle.

So, increased sensitivity, not necessarily so could have clinical symptoms or in a blood test. And the third criteria is polycystic ovaries. And when we look at polycystic ovaries, this is on an ultrasound, ideally a vaginal ultrasound, but the person has to be post-menarche more than eight years. So, if you've got someone in front of you who's 20 and have come in with, "Oh, I've had an ultrasound and I've got polycystic ovaries on ultrasound, but my menarche was 15," sorry, that's not going to be accurate because, like, up to 80% of adolescent girls have polycystic ovaries on ultrasound.

So, it leads to an over-diagnosis. So, it's absolutely not recommended if they're not eight years post-menarche. And very importantly, you have to rule out other etiologies. What else could be causing the anovulation or the oligomenorrhea? Could it be a thyroid condition? Could it be high prolactin? Could it be other causes that need to be looked at? So, the blood tests need to include looking at other factors that might be contributing to that picture in front of you.

Lisa: I'm so glad you mentioned that because I think on the Rotterdam criteria, the bit about high prolactin and hypothyroidism it's in, like, font four or something very small writing. And I think I have so many patients that present with anovulation and a diagnosis of PCOS and they have not had their thyroid checked or the prolactin. And when we do this, often there is coexisting thyroid, dysfunction or high prolactin. So, I think that is really important for our pracs to note down to get those tested.

Lisa: You were talking about the androgens before, if I take a little step back, about sometimes they're not elevated on the bloods. Are you talking about free testosterone and DHEA?

Sandra: So, any of them. So, generally, when you have a blood test, so testosterone is tested, sex hormone binding globulin. And that allows for a free androgen index, that allows for what I call, like, the misbehaving testosterone to be measured. And it's really important that the person has been off the oral contraceptive pill for at least three months because, of course, the estrogen in the oral contraceptive pill will suppress the testosterone production and increase the SHBG and it'll give a false reading. So, you know, this is also important to raise that the pill...some patients have been on the pill since 15, 16 because of acne, and then they stay on it for contraception and they come off it in their mid-20s, 30s, and all of a sudden they think, "I've got post-pill amenorrhea." But if it's any more than, you know, three months after the pill, it needs to be investigated for other causes. And partly this could be PCOS, which would've been very nicely managed by the oral contraceptive pill.

Lisa: Yeah. Do you ever test androstenedione?

Sandra: Not generally, but I do see it tested in the specialists and some of the GPs. And I don't routinely do DHEAS. And some of the specialists do. So, normally I would, you know, refer off and have these tests done. And it may have some impact, but because the classic diagnosis. And I know the specialist will often consider those androgens, those adrenal androgens as part of the criteria if the typical testosterone and free androgen index and SHBG are looking normal.

Lisa: Okay. Now, you talked a little bit before about the insulin resistance as being a common kind of denominator between the classical and the lean. What are some other things in terms of symptoms that the lean and classic might, I guess, differ in?

Sandra: Well, in fact, the research shows that most of the time they're very comparable, so you get similar prevalence of menstrual dysfunction, hirsutism, you get similar symptoms of also endometrial hyperplasia. And this is something really to point out if I can just go back. Because you're having these anovulatory cycles, it means that you're having these cycles where ovulation hasn't taken place, then we don't have the progesterone production, which is going to have an impact on stopping that proliferation of the endometrium. So, left unchecked, you get this estrogen building up and thickening the endometrium, and there's a risk of endometrial hyperplasia.

So, one of the benefits of having an ultrasound as well as to check the endometrial thickening, and this is what I call not estrogen dominance but unopposed estrogen. So, you've got this unopposed estrogen as a consequence of anovulation. So, still the drivers of insulin and androgen. And yes, you might have an unopposed estrogen, but, yeah, you've gotta keep that in mind. So, the general rule of thumb is if the patient is not having four bleeds, vaginal bleeds a year, they possibly will. And if we can't get these four bleeds a year, they may need to be sent off for, like, a progestin to have a withdrawal bleed. But there seems to be very similar sort of symptoms in terms of the hirsutism, similar hematological levels, like, similar LDL and cholesterol. Everything seems to be very similar. I don't know whether you've come across anything that shows that there's differences, but the main difference is their weight.

Lisa: Yeah, no, I agree. I think it's always a bit of a shock to practitioners and something for us to be aware of because I think we often maybe worry more about that obese patient in terms of issues with fatty liver and diabetes type 2, but actually, the lean PCOS seems to have the same sort of risk factors even though they're not obese. So, it's more about that insulin being the problem rather than, even though...

Sandra: Absolutely.

Lisa: ...they're not obese. So, I guess, building upon that you talked about the LDLs and the lipids sometimes being higher. What other comorbidities do you see with PCOS? What else do pracs need to be aware of and...

Sandra: Absolutely.

Lisa: ...screening for?

Sandra: Good. Yeah, that's a great point. So, you know, the 23-year-old in front of you worried about their acne is not thinking about having diabetes later on, but there is this unfortunate progression that goes to increased risk of gestational diabetes. And I see this so often.

Lisa: Yeah, me too.

Sandra: Like even someone who's with the PCOS patients, it's like, "Oh, my goodness, I'm doing..." And I think I've kind of mastered it recently, and I'll talk about that.

Lisa: Tell us.

Sandra: Well, I think just a spoiler alert, myo-inositol, I think is really... And I want to really talk about that later on because... I'll get to it because then I just want to mention these guidelines that have come out in 2023, which actually in the medical guidelines do incorporate myo-inositol. I'll talk about that and remind me. But yeah, absolutely, there's this progression of increased risk of gestational diabetes, increased register of type 2 diabetes, and that means it's cardiovascular risk. So, it's really all the way along. So, particularly, the older the patient, the more you have to screen for and you need to look at the lipids, and you need to look at the insulin, well, not so much insulin, blood sugar and HbA1C but definitely you mentioned fatty liver, which has now been changed. The name has now been changed to...as from June of this year to metabolic dysfunction associated steatotic liver disease, so MASLD...

Lisa: Oh, my gosh.

Sandra: ...which I think the fatty liver was a little bit too much sort of emotive sort of... So, it's a non-alcoholic fatty liver disease, is now metabolic dysfunction associated steatotic liver disease, MASLD.

Lisa: Oh, gosh, mouthful.

Sandra: I know. I thought you might like that. And they've got like a...and then you can, of course, there's a new category, of course, with the alcohol one in it as well if you're having any more than 140 grams a week. At 220 grams a week for females, that's something else. But yeah, absolutely. Like, that is a whole kind of progression with that metabolic sort of dysfunction that happens as a result of the insulin resistance.

Lisa: I think, you know, fatty liver is a really interesting thing in that lean PCOS, because again, it's not something you would associate with someone who has a relatively healthy whole-food diet. And it just really shows us that it's the insulin rather than, you know, poor diet. I found it really interesting reading about that, thinking that we often think about insulin kind of being the transporter of the sugar into the cells, but it also helps with lipolysis. So, in that insulin-resistant state, we see that then we get that increased delivery of those free fatty acids to the liver, which then leads to the... I'm going to call it fatty liver because I can't remember what the big term is.

Sandra: Absolutely. And look, we know as an aside that 15% of lean and Australian males have got fatty liver. And you wouldn't know unless you've kind of... So, yeah, it's more about just the fat, but it's the insulin that absolutely needs to behave itself.

Lisa: Now, we talked about before when we were talking about the diagnostic criteria, that there can be that hypothyroidism, Hashimoto's linked with PCOS. I know there's a huge number of meta-analyses and systematic reviews looking at that link. Do you see that a lot in your clinic?

Sandra: Yeah, it's interesting. I don't. I don't see it. So, I'm really interested in your input on that.

Lisa: Yeah.

Sandra: I do unfortunately see a lot of PCOS with endo, which is really two totally different conditions and we treat them quite differently. And I don't know why that's coexisting because we have to sort of target it. But no, I don't actually see the Hashi associated with the PCOS. Is that in your younger patients or older patients?

Lisa: I see it a lot with younger patients and, yeah, within the research, there's a lot of links showing that women with PCOS have higher TPO, thyroid peroxidase antibodies compared to controls. And I think a part of the hypothyroidism kind of picture is that you need T3 for ovulation to take place. So, if you don't have enough T3, then, obviously, you're going to have the cysts on the ovaries and anovulation. So, sometimes for me, it's just about increasing that T3, and then ovulation takes place and it's...

Sandra: That's interesting.

Lisa: Yeah. That's all that's going on. So, yeah.

Sandra: Yeah, yeah. it's interesting. There's some research with myo-inositol and Hashimoto, which I could never get my head around. And that now possibly if there's a similar, like, you know, certainly using it for the PCOS patients, it's sometimes difficult to get the thyroid antibodies tested where you kind of really have to push for it. But that's an interesting one that I'll need to look out for a bit more. While they're thinking about screening, one of the other things that is often measured, and it's usually the specialist rather than the GP that tests for this is the 17-hydroxyprogesterone.

Lisa: Okay.

Sandra: And that's particularly tested if you've got someone who's really quite hirsute. It's a symptom of androgenic cyst. And that's really to rule out any sort of late-onset adrenal hyperplasia or a tumour because we have to rule out those unusual or rare conditions as well.

Lisa: Absolutely. Is that something you've ever come across in your clinic?

Sandra: No. No. But all the specialists routinely tested.

Lisa: Yeah.

Sandra: Just, in particularly, the young hirsute patient, just to make sure that it's, you know, to rule out that it is a differential diagnosis of an adrenal tumour or an adrenal hyperplasia.

Lisa: Yeah. Great. Okay. So, we talked about how weight loss is considered the first line of treatment for women with that classical PCOS. And it's obviously not something we want to do in the lean. What about dietary recommendations for lean PCOS women who don't need to lose weight? What are you usually suggesting around that?

Sandra: Yeah, that's a great question, because we still have to address this insulin resistance. But rather than lose weight, I will use a low GI diet, ensuring protein at every meal, but incorporating some low GI carbohydrates to ensure that they don't lose weight. We still have to get them eating in a way that's helping with the addressing that dysglycemia. And so often these patients, unlike yours, are sometimes eating pretty badly they, and so they will need a little bit of adjustment into what they're eating. And some of these patients have got, you know, five, six, sometimes eight serves of carbohydrates a day, so I would often limit that to absolutely maximum of three good low GI carbohydrates.

Lisa: Okay. And so were you thinking things like quinoa, like sweet potatoes, that sort of carb?

Sandra: Yeah, it depends on the patient. Sometimes if I'm really going from, like, a white bread eater to... I will even just use, like, the Baker Institute guide of the plate because they actually listed this really... I'm not going to reinvent the wheel where they've got half the plate of veggies, quarter of the plate of protein, and then they'll list the low GI carbohydrates. And so that might be quinoa or brown rice or limiting the sweet potato or they'll talk about legumes where that fits in. But certainly getting away from the white squishy bread.

Lisa: Yeah. Okay. What about the old flaxseeds? And it's our fave. You're famous for your juicy flaxseed muffins.

Sandra: Yes.

Lisa: I know you recommend them a lot in perimenopause for hot flushes, vaginal atrophy and that sort of stuff, but what about their use in PCOS?

Sandra: Sadly, there isn't a particular use for them, except if these patients are constipated and you can use them for that. Look, I must say this can be my opportunity to get on the soapbox about seed cycling, which is one of my bugbears as well, which is a gross extrapolation of a little bit of research on flaxseeds, which I do use to lengthen the cycle generally in patients who've got short cycles. I don't know where this seed cycling comes from. One person rehashes what the other person says. Look, probably, the reason people feel good on it is all of a sudden they're having some fibre and some good nutrients. But, no, flaxseeds I will use here as a good form of fibre, but not anything, particularly, for PCOS.

Lisa: So, when we are talking... I've just thought. I know what seed cycling is, but I just wondered, some people may have no idea what we're talking about. So, seed cycling is when, I guess, there's a recommendation to do specific seeds at different points of the cycle. Right? So, flaxseeds, is that in the follicular phase? And then...

Sandra: I don't know. I don't want to promote it. I want to show... Look, it'll probably do no harm, but...

Lisa: But no, definitely no. Okay.

Sandra: Well, it'll do no harm. It just annoys me. I know I'm feeling like, "See, I'm being like a grumpy old woman." It annoys me when we kind of... It's discredit to our profession, I think. And most of it is not necessarily us. It might be social media rehashing someone else's idea about this is going to sort your cycle out and it's like, "Well, probably it won't hurt."

Lisa: Yeah. Well, I mean, I think probably having a range of seeds, flaxseeds, sunflower seeds, pepitas, all that sort of stuff. But not just at specific times in the cycle, but just throughout the whole cycle, right?

Sandra: Yeah, I reckon. Yeah.

Lisa: Okay.

Sandra: And this is going to be good because they are low GI, they're high fibre. All the things that we know classically are going to improve the way that our insulin and blood sugar regulation works better. So, in that regard, yes, bring them on.

Lisa: Okay. Great. Well, good. I thought flaxseeds were getting a bit of a bad rap from you for a second.

Sandra: No, no way. They're one of my top five foods for women. They're still up there. Don't you worry about that.

Lisa: Okay, good. What about vinegar? One of my faves.

Sandra: Well, you know what? It's funny. I used to poo-poo the whole apple cider vinegar thing and, you know, students would be prescribing and I'd say, "Nope, what are you talking about?" And then, anyway, just recently I was reading a Medscape thing and actually it's showing...

Lisa: It's a thing.

Sandra: It is. It helps with the way blood sugar regulation. So, maybe I'll hand that over to you, tell me, Lisa. You see, I'm Italian, I just put it on my salad and I have been known to drink the vinegar and oil at the end of the salad, but, like, now I'm being more open to the apple cider vinegar.

Lisa: Well, there is a lot of research on vinegar. It's been studied a lot for type 2 diabetes. Again, we're seeing meta-analysis, systematic reviews, but if we kind of take on the mechanism of action of what it does in type 2 diabetes, and it's there, it's improving insulin sensitivity. And it's the acetic acid component that basically delays emptying of food from the intestines, thereby helping balance blood sugar and improve their insulin sensitivity. They've also done studies in type 1 diabetes and also there's a couple of studies in gestational diabetes. So, I think it's a similar sort of thing that we see in the PCOS woman where that insulin is the issue that giving vinegar has been shown to help. Now, I'm talking this up a little bit, but there's only been one little study in women with PCOS, very small...

Sandra: Oh, that's good.

Lisa: ...seven, seven people. So, you know, not the best in terms of rigour, but, basically, they were consuming, I think it was something like 30 mils of vinegar, so not a huge amount of apple cider vinegar. And it helped to regulate that FSH, LH balance. So, it decreased the LH, which then resulted in less of those high androgens. And it improved ovulation, I think, in four out of seven of those women within three months. So, you know, you are looking at about a 50% kind of working there out of those women. But it's kind of cool because vinegar's so easy...

Sandra: Wow.

Lisa: ...to do. And I also like the way that... You said you have it over your salad with a bit of olive oil, because I think that's a lot more enjoyable, a lot more tolerable than having it in the warm water, which a lot of people kind of struggle with. It's quite burning and sharp, first thing in the morning. So, yeah, doing that with your food I think is great for any woman that has PCOS.

Sandra: What sort of doses, Lisa, do you remember what it's being used?

Lisa: Yeah, I think they talked about 15 grams of apple cider vinegar. So, I think that's literally only like a... I usually suggest for my clients doing a tablespoon with your salad at lunch and at dinner.

Sandra: No. One of my favourite aunties, so, we would wait at the end of the meal, she would grab the salad bowl because we're Italian, so there's always a salad. And we would watch and then she would pick up and she would eat. And of course, drink the rest of the vinegar, the vinegar and the olive oil. And of course, we'll have olive oil and we know how good olive oil is. So, maybe that's what we should be doing, just picking up the bowl and drinking the salad.

Lisa: Oh, yummy.

Sandra: But we have to do the salad before the meal, don't we? Now for the helping with the...and you drink the vinegar and oil. Yeah, that's easy.

Lisa: Delicious.

Sandra: I'm converted.

Lisa: Okay. So, we've got the lean PCOS woman sitting in front of us. Treatment aim, centering around, improving insulin sensitivity, down-regulating the androgen synthesis. We're not going to worry about the estrogen. We're giving vinegar, maybe some flaxseeds. And tell us about the myo-inositol that you were talking about before?

Sandra: Yes. Okay. So, let me talk about, first of all, these new guidelines that have come out. This is the update of the 2018 ones. But basically, Australian researchers and clinicians are quite prominently featured in it. And the difference between the 2018 and the 2003 version is in the first one myo-inositol was considered experimental, but they had dedicated quite a lot of information to myo-inositol. And so inositol is a secondary messenger and it has a role in insulin signaling transduction. And so it helps promote glucose uptake, which is what we want. And interestingly, they quote here that it's also involved in FSH-mediated pathways, which impact the proliferation and maturation of the granulosa cells. So, they've really gone into it. And while some of the things they talk about are still a little bit experimental, they've got studies that are comparing it to metformin with the way that it helps cycle regularity with less side effects. They quote the use with IVF and certainly in terms of helping with fertility. Now, it's important to think about when we look at PCOS patients as talking about subfertility, not infertility. These patients are not infertile, often reinstating ovulation. Well, in the overweight patient is much easier in terms of that weight loss. But, yeah, it's a subfertility.

Lisa: I love that you said that because I feel like a lot of patients feel so disempowered, like, with the term infertility and it is just subfertility for a lot of these women.

Sandra: It is subfertility. Yes. So, look, it's an interesting one. Most of the studies are done on an Italian formulation that's combined with folic acid. And the dose seems to be around two grams, either daily or BD and well tolerated generally overall in terms of how it works in helping with that insulin and glycemic control. But some of the research looks at, you know, improving cycle regularity, looking at some of the... I think there's even studies looking at what skin improves. But certainly, it's the only complementary medicine that's mid-listed in these evidence-based guidelines.

Lisa: So, Sandra, can myo-inositol be used in combination with metformin? Do you ever do that in your clinic, like, someone's on metformin and you use myo-inositol as well?

Sandra: Yeah, that's a good question. I have done. Interestingly, I tend to go for alpha-lipoic acid. Rather than if someone's already on metformin and we're trying to not let them go up to the 1000 milligrams because often the gastrointestinal side effects like the diarrhea click in. So, myo-inositol is still kind of the new kid on the block, but it's got the best level of evidence. But going back, there was a very small study done on lean PCOS patients where alpha-lipoic acid was used. And of course, that's insulin-sensitising. And so we don't want to forget about that one. So, I probably tend to use that one with metformin and also in myo-inositol in isolation, not with metformin, but usually combined. I'll often combine it with our other typical chromium, magnesium, cinnamon, the things that we also know that help with our insulin-resistant patients.

Lisa: Fantastic. I mean, I saw a study where they gave teenage girls with lean PCOS and, I guess, you know, it's hard when you were talking before about when women are quite young and their ovulation isn't established whether they really do have PCOS, but they were looking at the women with lean PCOS taking metformin versus the pill versus both. And the women who were taking the metformin versus the OCP they had less metabolic dysfunction, which I thought was really, really interesting. So, it is something that can be given to those younger women too?

Sandra: Yes. It depends if they go and see a gynecologist they get put on the pills, they see an endocrinologist, they get put on metformin. There really seems to be this kind of combination. And that's the same with us. What are we going to do? Do we address either or or do we address both? And the patient in front of us who comes in with acne we're going to treat differently to the person who's, you know, in their late 30s and wanting to get pregnant. So, you know, this, again, individual treatment, but, yes. So, often sometimes, depending on the pill, can often worsen some of those metabolic parameters.

Lisa: Yeah. Okay. So, we've talked about nutrients. What about herbs? Do you have any faves? I know with the classic, people tend to kind of gravitate towards the licorice Romania, but is that the same for lean PCOS?

Sandra: Yeah. So, again, it depends what the patient is wanting. So, if someone comes in, and they have acne, and I will just kind of look at the classic things that we'll be looking at diet and we'll use the...not necessarily use herbs. If I'm going to use herbs, I'm actually using alternatives. I don't think targeting the androgen type of mechanism with acne works so well. But the classic PCOS herbs are peony and licorice. Now, the peony and licorice, based on a Japanese study of this... Well, there was the similar formulas in Japanese-Chinese medicine and Chinese medicine. Peony and licorice helped to reduce testosterone and for cycle regularity. So, that's the classic combination. And our colleague, Susan Arendt, did a beautiful study using PCOS, one of probably the best studies that we have on herbs. Really well done.

Now, this was on overweight patients who were trying to achieve pregnancy, and she had a lovely control group where they were overweight and was just diet and exercise. So, that was really good. And it did improve ovulation rate and pregnancy rate. So, I wouldn't use peony and licorice for everything but if I am trying to work on cycle regularity, reestablishing ovulation and the diet and lifestyle hasn't worked, I will use that. And usually, I'm a non-Vitex user for PCOS, interestingly. It's two schools of thought. I'm Ruth Trickey trained. We definitely didn't use PCOS patients with Vitex. It tended to worsen cycle regularity. I know a lot of practitioners do use it and I just watch and look and I'm not ruling it out, but I tend not to use that as my first line of intervention.

Lisa: Okay. Interesting. I'm surprised to hear you say that when I know how much you love Vitex.

Sandra: Love Vitex. Yeah. I've got a sheet on to Vitex or not to Vitex. And everything's to Vitex. But, you know, is not to Vitex with PCOS.

Lisa: Okay. I also don't use it. What about black cohosh?

Sandra: It is. Interestingly, I think there was a study where PCOS patients, I think, they were having some sort of fertility intervention and black cohosh tend to increase the outcome, I think the pregnancy outcome. So, interesting one. So, I don't rule it out. It's not one that I use routinely.

Lisa: It's one that I use a fair bit for PCOS. I think, again, it wasn't really on my radar till I read that study that you're referring to. And they were talking about how black cohosh actually works for women with PCOS because it seems to decrease that high LH, which...

Sandra: Yeah, it does.

Lisa: ...I thought was really interesting. But again, they didn't use it in isolation. They were using it with Clomed, which is an ovulation inducer.

Sandra: Yes. That's trying with Clomed. But they also incorrectly referred to it as a phytoestrogen, so I'm not sure they have the full understanding of it. But we do know black cohosh lowers LH. That's a good point. And, you know, yeah, that's probably why it was important.

Lisa: What about St. Mary's thistle? Do you use that a lot? It's one of my faves.

Sandra: Not routinely, but, you know, the liver is important. So, I would probably tend to go more towards Berberis vulgaris because of the berberine, like, any traditionally herbs, bitters help with glycemic control. Now we know isolated berberine, really it's sold in China as an over-the-counter formulation that there's studies, comparing it to metformin with PCOS comparing it to the pill. So, I would tend to go to Berberis vulgaris rather than St. Mary's thistle.

Lisa: Yeah, interesting.

Sandra: It's kind of more of that traditional use of bitters working, and it will have a slight liver action rather than St. Mary's thistle.

Lisa: Yeah. There is a lot of research coming out with Berberis, for sure, the Berberine component. It's not something... I don't know why I haven't used it. It's something for me to think about. I like St. Mary's because of that fatty liver aspect. And I was thinking there's also good research coming out on it with regards to its ability to improve insulin sensitivity. So, that's where I was thinking of it for that.

Sandra: Okay. Yeah. Absolutely, with what we used to call fatty liver, yes, I would use that. Absolutely.

Lisa: What about adaptogens?

Sandra: Yeah, good point. Like, of course, we are looking at one sort of very important endocrine pathway, and we've got to look at the very second one that's important, which is, you know, that whole hypothalamic pituitary adrenal axis. Yes. So, adaptogens, like anything, we are naturopaths, we're going to look at the individual if there's stress going on if they're on this stress treadmill, adaptogens are going to be important to use.

Lisa: Yeah. How long do you feel like you need to use all these therapeutics to get an improvement with the cycle? Because some women really, really struggle with this irregular cycle ongoing for quite a long time. If you were going to forecast, what sort of timing would you usually see in your clinic for an improvement in regularity?

Sandra: My general rule of thumb is look at it over three cycles, but that's someone who has a cycle every month. So, someone who has a cycle that might be every 35 to 45 days, you might need to give it a little bit longer. And also you need to kind of consider these patients might be going on these medications for a longer period of time. So, if it's someone trying to achieve pregnancy, they might get pregnant, and then you just have to then continue to look after the cardiometabolic risk factors long-term. But I think it's going to be an individual sort of case-by-case, but, certainly, let no less than three months, you've really got to give it that amount of time, three to six months to see what the impact on cycle regularity. Anything to do with the hair. So, if you think about... So, hirsutism, any of the pharmaceuticals that work on that do not start working before 6 months and more likely 12 months. So...

Lisa: Wow.

Sandra: ...that's the most frustrating. So, I'm saying to a patient, "You're really going to have to take this for 12 months before we rule out that it's not having the full impact and whether it is having an impact." So, I think that's a good kind of one to consider.

Lisa: Definitely. It's good to get that idea in terms of the timeline because I think, probably like everyone, we kind of want results straight away, but hormones, unfortunately, doesn't always work like that, does it?

Sandra: No. Look, the hirsutism is a challenging one for patients because it really does impact self-esteem and their body image. And so mostly these patients are also going to be having some sort of laser or electrolysis. And if we're going to do it, so my...I tend to look at the zinc, I tend to... There's some research done on spearmint tea, interestingly.

Lisa: Yes.

Sandra: Yeah. But conversely, if they've got the female pattern hair loss, which is characteristically that widening of the part, I tend to use some saw palmetto, some serenoa. But again, you know, you really need to look at that over a longer period of time, 6 to 12 months. And I think we've got a...that's a herd that's untapped. There probably is an ovarian action with serenoa that we haven't really untapped, are tapped into. But, yeah, it's the hair, the excess, and the loss is longer term minimum.

Lisa: Okay. That is a really good tip because saw palmetto is typically, we think of it as being that prostate herb, right? But for female receding hairline you're going to be thinking about the saw palmetto. Excellent.

Sandra: Yeah, saw palmetto. It's a bit of an extrapolation on some research that was done on male pattern hair loss, which is a similar driving. And I think it was done topically. And I've used it and clinically it seems to make... It's probably one of the best ones we have for the female pattern hair loss, as well as, you know, we do have to make sure that these patients are having Biotin, like, two milligrams of Biotin is also important for the female pattern hair loss, and making sure that they're not low in zinc or that they're hypothyroid or that they're low in iron and all the other factors or they haven't had stress three months ago that is increasing their head hair shedding.

Lisa: Oh, my gosh. So many juicy tips.

Sandra: Yes.

Lisa: Thank you so much for joining us today, Sandra. You've really highlighted that while women with lean PCOS may have a different phenotype compared to that classical PCOS type that we know so well, they still demonstrate similar risk factors when it comes to things like type 2 diabetes, fertility, fatty liver, and so on. I think that's so important for us to remember as practitioners. You've given us some great tips on myo-inositol for us to use that with our lean PCOS women. And I couldn't finish without highlighting that last gem you gave us on saw palmetto for reducing hair loss. Thank you so much for joining us again today, Sandra.

Sandra: It's my absolute pleasure, Lisa. I love speaking to you. I love getting your insights into this. And my mouth is salivating at the thought going... We have some apple cider vinegar now.

Lisa: Thank you, everyone, for listening today. Don't forget that you can find all the show notes, transcripts, and other resources from today's episode on the fx Medicine website. I'm Lisa Costa-Bir, and thanks for joining us. We'll see you next time.

Emma: This podcast is intended as healthcare practitioner education only, and it is not a substitute for medical advice, diagnosis, or treatment.


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