The Estrobolome is the totality of all metabolism and conditions related to oestrogen. From common complaints such as acne to devastating oestrogen-driven conditions, the estrobolome is sensitive to external factors which Moira Bradfield is expert in managing. In today's podcast, we delve into the substrates, biochemistry and naturopathic management of oestrogen-related conditions. Moira shows us how to assess and test for issues, and how we can effectively balance the estrobolome to bring about positive changes in oestrogen metabolism.
Covered in this episode
[00:56] Welcoming back Moira Bradfield
[02:06] The estrobolome and its influencing factors
[09:42] Types of oestrogen and risk of disease
[14:16] Pathology testing
[17:06] Inhibiting deconjugation pathways
[21:47] The importance of fibre
[23:56] Using diindolylmethane (DIM) and indole-3-carbinol
[30:09] Lifestyle recommendations
[33:15] Additional resources for practitioners
[34:34] Closing remarks
Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook. Joining us on the line again today is Moira Bradfield. Moira is a naturopath and acupuncturist who's been in clinical practice for over, I think, 17 years now. Graduating with a Bachelor of Naturopathy from Southern Cross University in 2001, Moira has worked as a naturopath in a variety of settings with a wide range of health conditions and disease states.
In the pursuit of blending naturopathic medicine with oriental modalities, Moira completed a Diploma in Traditional Thai Massage in 2004, and in 2010, completed a Master's Degree in Acupuncture, through, again, Southern Cross Uni. She now incorporates effective oriental protocols into her naturopathic practice. She's travelled to the United Kingdom, Thailand, and China as part of her clinical training and interest in oriental health. Moira blends this passion with a solid biochemical and pathological framework to create relevant and effective approaches to health and healing. Welcome back to FX Medicine, Moira, how are you going?
Moira: I'm very well. It's a pleasure to be back.
Moira: So if we break “estrobolome” down, which is what I like to get my students to do, and we look at the suffix of it which is “o-m-e” or “ome,” which in molecular biology tells us that we're looking at the totality of some sort. So we're looking at the totality essentially, of oestrogen and oestrogen metabolism with a focus on the microbiome, essentially, in the human body. And how that's actually interacting with oestrogen.
Andrew: So obviously we're talking about gut health here. We often overlook that. We tend to sort of compartmentalise the hormone as the hormone, without regard for how we metabolise the hormone. Let's go through these major influences, though. So what are the major influences on the estrobolome?
Moira: So we're talking about… You're right, we're looking at gut health, again, and the many influences that microbiomes and their genetic or their gene components and what they actually code for and produce. And then how they interact with the human organism, and how the human organism is also feeding itself. So all of that will have flow-on effects into the interior of the body or the endogenous aspects of how we also metabolise and clear.
So we're looking at the gut, we're looking at the liver and the enterohepatic recycle of oestrogens. Which has always been an understanding that we've seen throughout the years, in that there is… We know enterohepatic recycle of oestrogen occurs. In fact, I remember teaching pharmacology many years ago and talking about the oral contraceptive pill and how enterohepatic is part of the equation of steady-state dosing with oestrogen in contraceptives.
So it's not that this is new knowledge. It's that actually we've developed now more in-depth understanding all the influences on the microbes which have this set of enzymes, which are, well there’s a few of them. The ones that I've mostly focused on, the beta-glucuronidase and the glucosidase enzyme systems, which are involved in the deconjugation of oestrogen at the gut level.
And so there was obviously a lot of influences on how that might be occurring and which microbes express those enzymes, more or less, and what that actually might mean. So there's, from our understanding on oestrogen and its metabolites, we know there are a lot of influences on a liver-based level. And certainly, these conjugates are coming from liver, from Phase 2 detoxification.
So we're looking at that being obviously pumped back via bile back into the intestines, and then being acted upon via microbes. And certainly, we're looking at whether some of that ends up down the toilet, or whether it's there and available to be reabsorbed.
Andrew: So when you're talking about beta-glucuronidase and beta-glucosidase systems, should the major impact be from our microbiota? Or is the major impact on dietary influences? Or is it equal?
Moira: I think that we can't really separate the two. So, we know, obviously, that dietary influences are varied in that we see expression of these enzymes influenced by diet, by fibre content, by fat content, by protein content, and that those things… So for example, in a vegetarian or a plant-based diet, we actually see a decreased expression of their beta-glucosidase and beta-glucuronidase, and a higher faecal excretion of oestrogen conjugates, so essentially clearing it from the system more effectively. And in higher fats and higher protein diets, we see the reverse of that. So we see a higher conversion or a higher deconjugation of these oestrogen metabolites, and less of that available in the stool. And that certainly makes sense when we're looking at the role of fibre as a substrate for microbes to actually work on, and also as a tool to improve diversity within the gut.
So, we see that in the microbe world, there is actually you know, over 60 different types of genus-level bacteria that we can look at that have the ability to produce either both or one of those enzymes in variant circumstances. And not all of those are bad. Certainly, lactobacilli and bifido species, which we normally call the “good guys” are in that category and have that propensity to be able to produce those particular enzymes.
But it's about the diversity score, essentially, because once you start decreasing the diversity, which we know there's a range of influences from exogenous and endogenous sources… As you start decreasing that diversity, you certainly have a higher expression a lot of the time of these enzyme systems, and you have less of the helpful things that we would consider involved in the clearance of them from the system. Which is essentially, binding them at the gut level and putting them down the toilet instead of allowing them to be taken back up into the body in higher amounts and adding to that oestrogen burden that we see.
Andrew: It's a very interesting point you make about how the foods that we eat are used as substrates for our bacteria. And obviously we need to diversify those. It offers another level of action on good old fibre rather than just the fibre as a physical entity binding to a hormone, but itself being used as a substrate for a more active, if you like, production of enzymes or controlling enzymes, which can help in hormone regulation.
Moira: Definitely. And I think that's where we're getting to as our level of understanding increases in terms of microbe diversity in the gut, where we aiming for a higher diversity being associated with a state of health, that we know that different fibre types, different, you know… A greater diversity of different types of plant foods is associated with greater influences on health.
And I don't think we can separate the fibre component from the other phytochemicals that we see coming in when we look at a, you know, a good whole food plant-based diet. Because certainly, the phytochemicals have a role as well. You know, in amongst that when we look at a lot of those foods that are touted to be superfoods, so the green leafy vegetables for example, and the bright colourful fruit, we see the ability to have calcium d-glucarate as a component of those foods naturally occurring, which will also interact with those enzymes and inhibit, particularly the beta-glucuronidase enzyme.
So we've got natural things that come in. And those foods are often packaged as well with the components that will influence both Phase 1 and Phase 2 liver detoxification. So, again, we're looking at this totality of interaction from a food or a particular food source that influences health in a positive way. And when we start breaking it down to influences in a research-level, which is often what happened, you know, if we go back and look at things like breast cancer, you know, that they would associate obesity or they associate alcohol or they associate, you know, protective or negative effects from different behaviours.
Now, with an increased understanding of the estrobolome, there's another depth of what might actually be going on and why that is a risk, or why that is protective. And we also understand when we see quite counterintuitive things, you know, like the protective roles for example of cigarette smoking, when we're looking at that in terms of, you know, some oestrogen cancers, whereas obviously, it's a risk for other types of cancers in, you know, people. So it's about what that actually might be doing to these microbes and their expression of these particular enzyme sets, and how that influences oestrogen.
Andrew: I also take the point that, as you said, commensals. Some commensals might be the glucuronidase. Two things here, I guess. One is the practicalities of good old “keeping your bowels moving.” The other point I've sort of taken from a few things you've said before was… We've spoken about estrobolome as if oestrogen is one entity. And of course, it's not. Can we just branch into the different types of oestrogen and what may be their risk is or their importance in disease?
Moira: Yeah, definitely. So we certainly have different types of oestrogen at different stages of life as well, and if we take a female as the example in that, and granted, males obviously carry oestrogen, but we often talk about it only related to each time to females…
Moira: …as the main subset of clients that many people will see. So we have oestradiol which is E2, and that's predominant in non-pregnant people and definitely prior to menopause. Oestrone, E1 which is predominant after menopause, and then is oestriol which is E3, and that's high during pregnancy.
And then we have the ability to interconvert some of those forms of oestrogen, so certainly oestradiol, so E2 and oestrone E1 interconvert to each other via Phase 1 enzymes. And then via Phase 1 and Phase 2 detoxification… So we're talking about functionalisation reactions via CYP enzymes and conjugation reactions via a substrate. We have then the further conversion of oestrogen down into metabolites. And many of the listeners may be familiar with, you know, or they learned at school, for example, that we have the 2-hydroxy oestrogens and the 4-hydroxy oestrogens and the 16-hydroxy oestrogens and they will be further converted into methyl or catechol forms of oestrogens.
But the reality is that we're talking about quite a long carbon molecule. Eighteen carbons in oestrogen, or an oestrogen form and that the carboxylation, you know, can occur on any of the carbons on that molecule. And that's where our 2s and 4s and 16s are coming. So there are 1s and 2s and 3s and 4s and 5s, and, and so on right up until 17 and in each of those categories, we have a range of metabolites.
And our understanding of those is really unknown, you know? These things, obviously, being metabolites, we know when things go through detoxification reactions or through the liver, that the fate of something here is that it's either become less active or it becomes more active. And it depends upon what's acting on it, and what else acts on it after that. But the ultimate goal of those phases of our liver detoxification is to make something more water-soluble, so that it can be excreted. You know, that things are reaching, obviously, half lives and are moving through and continue to do that on a daily basis as we produce and interact with different cells.
So excretion, obviously, is the end part of that metabolism pathway, and we also need to look at that in the sense of a naturopathic or a holistic perspective. Are people excreting and what pathway are they doing that from?
And these things being water-soluble, we have a variety… Well, depending upon how water-soluble they are, whether they come in through bile or sweat, or, you know, lactating them out, spitting them out, spilling them out, weighing them out, you know, the possibilities are endless. But they're all different types of metabolites.
And we focus in on the 2 and the 4 and the 16, because there's a lot of research on how they may actually be involved in disease and also being protective. Particularly in relation to things like oncogenesis with breast cancer, because of the fact that we associate, you know, the 2 form with being less or antiproliferative, and the 4 and the 16s as potentially being more proliferative in terms of their action and their ability to bind to and initiate cellular proliferation in different areas in the body where there are oestrogen receptors.
Andrew: Yeah. And indeed, you know, moving on from there when you're talking proliferation, we don't just have to be talking about a cancer. We can indeed be talking about the influences on endometriosis, the influences on things like hemangiomas. I've seen really good results with that, strangely. I'm very interested also in the sort of oestrogenic aspects of bowel cancer proliferation. So we tend to sort of compartmentalise it into a sex hormone or a sex organ type thing, and it can indeed have influence on other organs as well.
Can I just ask though, you mentioned before about CYP enzymes, and obviously we're going to be talking a little bit, we always will reflect on the genetic influences here on oestrogen metabolism. And I guess I'm talking here about, you know, your CYP SNPs. How strong or relevant do you find they are or do you just look at pathological testing or functional pathology?
Moira: So they are relevant, whether you need to test them or not, is entirely optional, I believe. So certainly we have the ability if we’re looking at oestrogen metabolites to test that. We also have the ability to look at oestrogen profiles and break it down into E1, E2, E3, and from that, you can sometimes work backwards.
Certainly, the age of genetic understanding does offer some aspects of personalised medicine, but I also realise the drawbacks in that. So certainly, if we are seeing higher amounts of the 2-hydroxy, our assumption then is that the CYP1A1, 1A2 enzyme systems are working effectively. Or if we're seeing the 4-hydroxy forms of CYP1B1 or the 16s as CYP3A4. And we also know that there are a variety of influences on those in terms of exogenous input. And that includes pharmaceuticals as well, how we may actually be inducing or inhibiting the expression of those enzymes.
So you have to look at the totality of a case history. I don't personally do a lot of genetic testing because I find that I feel overwhelmed very quickly. And then when I step back and look at the totality, it makes more sense for me. But there are influences even further downstream on a genetic level, because certainly when we look at 2 and 4-hydroxy oestrogens, they are further metabolised to relatively inert and possibly anti-carcinogenic compounds via COMT. And we do know that catechol-O-methyltransferase does have variability as well and that there are underactive and overactive forms of that.
And so whether if that's underacting, then we've got a higher propensity for those two types of hydroxy oestrogens to actually become free radicals and travel down a more oxidative damage pathway, which is a quinone based pathway. So we actually, you know, if anything, COMT is probably very important to look at, if we've got information on the twos and the fours, and we want to see what's actually happening. Because the two methoxys, which is the next step when you've gone through the catecholamine methyltransferase is, you know, the twos and the fours of the next step. So understanding that level of variation in SNPs is possibly advantageous to the practitioner as well.
Andrew: We've spoken about fibre having its action on inhibiting beta-glucuronidase and beta-glucosidase enzymes in breaking apart a conjugated oestrogen, and therefore allowing the oestrogen to recirculate. Are there any sorts of things that you can give a person as an intervention that might override these deconjugating enzymes?
Moira: Yeah, definitely. I mean, fibre, obviously, and food. I mean, there are so many beautiful foods that naturally contain these compounds, you know? And in fact, there's research that tells us if we just have a diet that's 4% component of that, which is not hard to achieve when we look at the variety of plant-based foods that these, you know, components like calcium D-glucarate, and glucaric acid actually occur in, that we can achieve that and actually be influencing glucuronidase expression.
And then we can look at that on a level of calcium D-glucarate, which can be breaking locally, but also systemically. We have things like DIM, which is a possibility as well to influence glucuronidase. Rosemary, if you're looking at therapeutics will also inhibit beta-glucuronidase.
So there's a variety of things that we already use and have used for a very long time for oestrogen, relative oestrogen dominant states that now are being found to have this action. The interesting thing when we start looking at them, and granted a lot is mice studies, is that there is also some quite unpredictable things that go on with microbes as well, with some of the things.
So if we take rosemary, for example, you know, you can actually affect some of those more beneficial microbes and decrease them because on some levels it is an antimicrobial, and then favour some more, what we would consider to be pathogenic microbes and these in rats and mice and ruminant studies that I've seen this actually occur. But overall, if we're taking rosemary in, you know, food and how we might prepare it and how we traditionally would include rosemary, which is with higher fat foods, which would be inducing beta-glucuronidase as well, then that inhibition is actually warranted in that circumstance.
Or, again, the other things that we sometimes shy away from like grapefruit which has naringenin, which is, as we know, is a lowered of Phase 1 detoxification, so actually inhibit the CYP enzymes, but overall, it has limonin in it, and it has fibre in it, and it can also impact beta-glucuronidase. So these are all quite, you know, balancing effects overall if we are eating them in a whole food complex form, which is how I tend to address these.
And then we have some more, sort of, specified targeting things where you can look at the balance between Phase 1 and Phase 2 detoxification and what might be influencing that and take away influences, particularly on glucuronidation and sulfation, because this is how we actually metabolise those oestrogens in that Phase 2 detoxification.
Andrew: Obviously, the only caveat there with grapefruit is A: get a good one. But B: be mindful of any medications that you might be on and take heed of any warnings that are present.
Moira: Oh, definitely. Yes, because, obviously, inhibition is a problem when we're wanting to clear. I mean, it could be a problem if that's all you were having as well on an oestrogen level because you were completely going to change how that's metabolised in the body, and not necessarily in a favourable way in that you would end up with higher amounts of circulating estradiol and oestrone. And they can, obviously, have potential health repercussions as well. So looking at ways that we could favour oestrogen metabolism down to the two hydroxy forms, and to the two methyl o- forms, then those are the things that may have longer-term outcomes. But we are essentially then decreasing active oestrogen as well. And that's not always suitable for everyone.
So this still needs to be personalised medicine. And granted this issue that you mentioned before, that the impact of oestrogen obviously, it's not just on cell proliferation in oncogenesis, that it does impact obviously uterine tissues and other tissues, breast tissues and things like that in the body. And we need to consider that as well, in that we can modulate and affect benefit, but we can also possibly push things too far if we're not considering the other levels of interaction that occur. And so sometimes if we're interfering with how something may be hydroxylated, we can actually induce, if we're not considering COMT, we can induce things like anxiety, which obviously is not a great outcome for your client either.
Andrew: Not a great outcome. Now, you've mentioned fibre before, I think we need to delve a little bit further into that, because you've got different types. You've got different, you know, on the gross level, you've got soluble versus insoluble, but then you can also go on a micro level and talk about the different molecular lengths. Can we discuss that a little bit? Do you favour one over the other?
Moira: Sometimes I favour one over the other if I have a snapshot of what might be going on with the microbiome. So if there's some sort of genomic information that I have, then that would dictate to me what type of substrate or prebiotic fibre I might actually be using for the colonic bacteria in terms of, you know, encouraging what's going on and changing ratios around that. But in an overall look at it, it for me is purely about increasing the diversity of plant foods in somebody's life.
Because when we look at it and someone will sit down in front of me and say "Oh yeah, I eat vegetables," and dietary recall then reveals that the vegetables are in their evening meal and consists of a cup overall and maybe a few spinach leaves at lunch underneath a piece of fish, then that's not necessarily for me the amount of vegetable nor fibre that I want in somebody's life.
So all of those things that, you know, insoluble, soluble, and resistant are important in the interplay of what might be going on, because we have them being substrate and fuels and, you know, inducing short-chain fatty acid production and butyric acid, and all of those beautiful things that we find to be preventative for some types of issues in health. And we also are requiring, if we're looking at things like calcium D-glucarate and also in also indole-3-carbinols, which we find in those cruciferous and Brassicaceae family, that there has to be a certain level of acidity for them to be able to convert as well.
So we want to encourage healthy short-chain fatty acid production, healthy digestive processes, so that we can optimise any therapy, whether it be supplemental or dietary that we're putting in play for that particular person.
Andrew: You've previously mentioned DIM, diindolylmethane, and you've just mentioned indole-3-carbinol. Can you give our listeners a rundown on how they're similar, how they're different, and what are the issues facing these two nutriments and particularly in supplemental form?
Moira: Yeah, so indole-3-carbinol is produced by members of the cruciferous family. So we're looking certainly at cabbages, radishes, cauliflowers, broccoli, Brussel sprouts…
Moira: …daikon radishes, all of those beautiful things that we want our clients to be eating anyway. And many of those have the calcium D-glucarate that we also want to be supplying and can affect directly aspects of Phase 1 and Phase 2 liver detoxification. So all around fantastic foods to be including. And if we focus on indole-3-carbinol, so this is an isothiocyanate. So it's a sulphur-containing molecule within our cruciferous family and that's a lot of them, that's what they're known for. And it's conversion under acidic conditions is to DIM. And so there's a lot of research on both of those compounds.
And when we look at the research surrounding indole-3-carbinol, which is varied from everything to do with androgens to specifically oestrogen, cancer risk… We have an understanding that some of the benefits that we're seeing in those research when they're looking at I3C is actually because it's converting to DIM. So on a clinical level for me, if I was choosing between the two, I actually want the one that I know is going to work more specifically. So I go towards DIM as well. I certainly have an understanding I'm going to be increasing the indole-3-carbinol on a dietary level, and therefore the body will be able to pick and choose where it sends it down its pathway of metabolism. But I want the DIM in circulation to have those quite specific aspects and action on the oestrogen conversion pathways.
And, you know, interrupting, depending upon the client and what they're actually coming in for whether we're looking at, you know, oncogenesis and cell cycles and how that might actually intervene. Because, you know, the more you go through that research, the more we realise that they actually are talking about DIM, even though they're labelling it or calling it I3C at the beginning. I mean, there is always a conversion and there are other metabolites granted from that starter compound, and certainly we can't overlook the fact that they may be having actions that we're not aware of as well.
But in terms of the anti-oestrogenic effects and the interventions that the oestrogen receptors and how those signals are transducing, for me, that is more to do with DIM. And therefore, if I'm trying to influence what's going on with hydroxylation pathways via those CYP enzymes, then I would go down a DIM pathway.
Andrew: What about things like broccoli sprout extract though, do you find that it can have a major effect clinically on oestrogen balance or oestrogen issues with your patient?
Moira: Personally, not a major effect. So I have had clients where we've done DIM and then we're moving into say, a conception phase, and for me, I don't necessarily want something in play that I'm going to have to drop if conception has occurred. So I would want a much more, you know, subtle regulation of hormones. So I will use broccoli sprout extract in that way. It has an effect.
Granted, it has an effect, as, you know, because we're looking at a more concentrated form of these vegetables, but it doesn't seem to influence those ratios in quite an extreme way we're looking at over time.
But if you are playing and manipulating on multiple parameters, then certainly broccoli sprout extract is a valid intervention. But I would want to be looking at what else is going on, what else is influencing the functionalisation reactions, but also the conjugation reactions. And certainly, making sure that these people are pooing regularly, that fibre is adequate, that we've got bile being bound and put down the toilet and not being allowed to sit, you know, and have that opportunity to be acted upon by microbes so that it's reabsorbed.
Andrew: One last point I just forgot to add about the use of DIM and I3C is if one prefers I3C, indeed, I would say do it for both. If you're using either of these in a supplemental form, then you really should be looking at doing a baseline test of oestrogen metabolites and also a treatment test, say three or four months later, and make sure that that test includes the four series of hydroxy oestrogens, so that you can show a shift. And whatever you're using if you can't show a shift, why are you doing, you know, why are you using that treatment?
Moira: That's right. This, I mean, I do some testing in clinic and I definitely test metabolites. It's one of the things I will do if I implement a treatment and we're looking at that. And then we will retest as well as we start. I mean, my whole precept in clinic is not to have people on supplements forever.
Moira: So there has to be enough lifestyle and modification in play that I can move somebody away from a supplement basis. And again, that would be part of a retest, and are our ratios moving? What is it that you're doing that's, you know, not compliant, because we have other inducers, you know, certainly alcohol is a huge inducer, not even non steroidal anti-inflammatory drugs most will affect sulfation. Food dyes will affect sulfation. Deficiencies of cofactors, molybdenum for example, will affect sulfation. If people are using aspirin on a regular basis, we're affecting glucuronidation.
So we have to make sure that those things are controlled for as well. Hopefully moving to an optimal place of health, rather than, you know, just using supplements, not changing lifestyle, particularly in this case, you know, what sort of xenoestrogen influences have we got coming in? What type of level on the body level is not clearing and metabolising effectively, and why? And how do we actually address that?
Do you practically tend to concentrate more on the dietary influences, the bowel moving properly, making sure that they're drinking enough water, and all of these really basic lifestyle things that we all should be doing, before you go gung-ho with liver herbs and dump a whole lot of bile out into the bowel and potentially overwhelm the ability of the fibre to conjugate that. How do you practically intervene here? And what does it show up as in your patients?
Moira: Yes, I do now. I think probably in my younger years, I would use herbal medicine that would be stimulating bowel flow without actually considering bowel elimination. But now that's the primary thing, you know, people need to be having a daily bowel movement, it needs to be the remnants of yesterday's food that are in that bowel movement, not last week's. And we need to make sure that they are clearing because transit time will affect what happens with those bile acids, whether they become secondary bile acids, whether they're reabsorbed, deconjugated, you know. And we certainly know that that will also change microbiome diversity, and that will favour bile acid resistant microbes and their influence on health and, you know, digestive symptoms, like IBS is quite huge.
Moira: And even things like the presentation of SIBO, which we probably need to talk about soon, you know. So, for me, I think that the going back to basics and making sure people are eliminating through their elimination pathways is the basis of oestrogen and dealing with oestrogen on this level.
And then the flow-on effects of that are that your microbiome should actually be able to adjust to that, and express itself in a way where the beta-glucuronidase activity is sufficient. Because even if you have a eubiosis, if you had a gut that is balanced and considered to be diverse, you have the enzyme production by these microbes. But if you're not clearing your bowels effectively, then you're always going to deconjugate. It just depends on to what level, and certainly, we know if you're not clearing your bowels, then you are actually going to shift towards dysbiosis.
And there's some interesting research out there looking at beta-glucuronidase inhibition with antibiotics. And you read it and you go, "Oh, that's great, you know, antibiotics do inhibit beta-glucuronidase.” Yeah, they do, because they're wiping out your microbes. But the longer you use the antibiotic, the more you shift towards a dysbiosis and the higher your beta-glucuronidase expression will be via the dysbiotic microbes, because we lose the diversity, which means we lose the balance between the producers and the non-producers. And then we team that with a dysbiosis with a motility issue, and we increase the equation more so where we've got bile hanging around for longer. So yeah, it's a primary thing, get these people pooing.
Moira: There are some papers that we'll make available. So even though the estrobolome seems to be a new concept, as I said, when you go back through the research, there is over 20 years' worth of information that points us in that direction. Within the last five years, we've probably got some more papers coming out with the catchphrase in it, which is estrobolome.
Moira: And then, certainly, a lot now looking at the influence of that on breast cancer. So there's some great breast cancer research papers out there with information. And it brings into good perspective, I think, as well, because we have this black and white thing where the 2s are great and the 4s are, you know, not great, and the 16s are even less great, but it talks about the fact that the 2s and the 4s can actually play inverse roles depending upon the situation. And again, that for me speaks of the need to have that person sitting in front of you assessed. So I will provide the links for those on the web page.
Andrew: And we will, of course, put these up on the FX Medicine web page for our listeners. And if people have any questions or indeed any controversies that they're coming up against, please contact us on the FX Medicine social platforms.
Moira Bradfield, thank you so much once again for joining us on FX Medicine. I love listening to you. I love the way that you always have like a patient that you're thinking of in front of you, and you're always cognisant of what's happening with them on a human level, not just a biochemical level. You're very mindful of their lifestyle and the, you know, affordability of supplements and you take into account their totality when you're treating them. I love that about you. That's why I admire you so much. Thank you for joining us on FX Medicine today.
Moira: Thanks for having me once again. It was a real joy.
Andrew: This is FX Medicine. I'm Andrew Whitfield-Cook.