Endometriosis: 10 Things You Can Do To Help

Summary

Podcast Summary: "A Gut Feeling — Endometriosis: 10 Things You Can Do To Help"

Host(s): Dave O'Brien & Jake Doleschal
Date: August 3, 2026

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Episode Overview

Dave and Jake take a deep dive into endometriosis, discussing 10 practical interventions that can help those recently diagnosed or struggling with symptoms. They blend perspectives from casework, recent research, and holistic health coaching. While not an exhaustive primer on endo physiology, this episode aims to empower listeners with actionable, evidence-informed options, particularly targeting pain, inflammation, hormonal imbalances, and gut health.

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Section 1: Setting the Stage — What is Endometriosis?

[06:17] – [11:26]

• Definition:
  Endometriosis involves patches of tissue similar to uterine lining growing outside the uterus—on ovaries, fallopian tubes, ligaments, digestive system, even lungs or appendix in rarer cases.
• Drivers:
  Estrogen is a major factor, hence the hormonal link. Other debated factors include bacterial dysbiosis, immune function, inflammation, and possibly autoimmune components.
• Prevalence:
  ~10% of women of reproductive age worldwide (about 190 million worldwide), though true rates may be higher due to diagnostic delays.
• Impact:
  Women with endometriosis often suffer profound, recurrent pain that can be debilitating—“bedridden for a week every month.”

Memorable Quote:

“The change that has on people's lives is astronomical... Being able to reduce that pain even by a few days a month is huge.”
— Jake [10:19]

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Section 2: Conventional Approaches and Why They’re Not Enough

[04:01] – [12:07]

• Medical standard of care:
  • Laparoscopic surgery
  • Hormonal suppression (pill, IUD)
  • Pain management (NSAIDs, opioids)
• Gap:
  These treat symptoms, not root causes or contributing mechanisms like inflammation, histamine, or microbial imbalances.

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Section 3: 10 Holistic Interventions for Endometriosis

1. Address Gram-Negative Bacterial Overgrowth & Histamine–Estrogen Loop

[12:07] – [21:16]

• Dysbiosis (notably SIBO, Gram-negative bacteria) is implicated via increased histamine and LPS (lipopolysaccharides), which drive inflammation and worsen estrogen dominance.
• Histamine amplifies estrogen activity and vice versa, creating a self-perpetuating loop.

Key Interventions:

• Stabilize mast cell activity: Quercetin, Palmitoylethanolamide (PEA)
• Bind LPS: Lactoferrin, dietary interventions
• Address SIBO: anti-microbial and gut support strategies

Quote:

“People just get stuck in this feedback loop: histamine, estrogen, more inflammation, more pain.”
— Dave [16:40]

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2. Leverage the Power of Beta-Caryophyllene & TA-1 (Thymosin Alpha-1) Peptide

[22:20] – [26:14]

• Beta-caryophyllene: Reduces both pathogenic Gram-negative bacteria AND persistent oxidative stress; shown in rat studies to shrink endometriosis-like implants by 52.5%.
• TA-1 peptide: Suppresses Toll-Like Receptor 4 activation, implicated in endo lesion growth. (Availability of TA-1 may be limited; beta-caryophyllene is found in certain supplement blends.)

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3. Adopt a Low-FODMAP Diet (at least short-term)

[26:43] – [29:09]

• Endometriosis often co-presents with IBS symptoms, likely related to microbial imbalances.
• Low-FODMAP diets reduce symptom severity but aren’t a cure—most helpful as a “symptom management tool while you fix underlying gut issues.”

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4. Support Estrogen Detoxification & Gut Health: Probiotics

[32:36] – [41:37]

• The estrobolome—certain gut bacteria—regulate estrogen metabolism. Dysbiosis upregulates enzymes (β-glucuronidase) that increase reabsorption of estrogen, worsening symptoms.
• Probiotic strains (e.g., Lactobacillus gasseri) may help modulate estrogen, inhibit proliferation, and rebalance the vaginal and gut microbiome.
• Probiotic suppositories (for vaginal health): an emerging area, but oral still helpful.

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5. Optimize Antioxidant Defenses

[41:55] – [47:55]

• Key insight: Endo is driven by chronic oxidative stress. The most powerful antioxidants are those produced by the body—melatonin and glutathione.
• Beta-caryophyllene and quercetin offer strong antioxidant and anti-inflammatory effects.
• Not all antioxidants are equal—don’t rely solely on diet-based antioxidants.

Quote:

“The most potent antioxidants are the ones you produce... look after melatonin and glutathione first.”
— Dave [44:50]

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6. Utilize NAC (N-Acetyl Cysteine)

[48:51] – [54:29]

• Precursor to glutathione, thins biofilms, and has direct anti-inflammatory and anti-dysbiosis effects.
• Clinical studies found NAC reduced endometrioma size, pain, and led to canceled surgical plans (“24 of 47 women scheduled for laparoscopy canceled after NAC”—[57:07]).
• Dosing varies; some use daily, others cycle, but both approaches have merit.

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7. Use Melatonin

[54:29] – [57:07]

• Powerful endogenous antioxidant; reduces lesion growth and pain.
• Human study: 10mg daily resulted in 40% reduction in pain scores [55:05].
• Might be especially relevant given LPS can degrade blood–brain barriers, taxing melatonin reserves.

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8. French Maritime Pine Bark Extract (Pycnogenol)

[58:06] – [62:26]

• Potent antioxidant, anti-inflammatory, and pain modulator.
• Research: Adding 120mg daily (with hormonal treatment) led to complete elimination of pain in 50% of women vs. 0% in the control.
• Also reduces heavy bleeding, spotting, and other secondary symptoms.

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9. Bind and Remove Heavy Metals: Modified Citrus Pectin (MCP)

[62:34] – [70:17]

• High levels of cadmium, lead, arsenic, and mercury linked to increased endometriosis risk (e.g., cadmium/lead increased risk three-fold).
• Modified citrus pectin (MCP) binds heavy metals and LPS, inhibits Galectin-3 (involved in endo lesion development), and doesn’t deplete minerals like other binders.
• Expensive, but “best fiber powder by a mile” for these clients.

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10. Iron Regulation and the Role of Lactoferrin

[70:53] – [76:21]

• Many women with endo supplement with iron due to heavy bleeding, but iron supplementation risks tissue overload, contributes to infection risk and worsens dysbiosis.
• Inflammation and LPS drive up hepcidin, trapping iron in tissue (low blood, high tissue iron; a paradox).
• Lactoferrin: modulates iron absorption, supports gut integrity, binds LPS. Safer and more nuanced than iron supplements.

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+1: Pain Management with PEA (Palmitoylethanolamide)

[77:13] – [80:34]

• Direct evidence in endo: reduces pelvic pain, painful menses, painful intercourse, and bowel pain.
• Works for many types of chronic pain with very few side effects; can mitigate NSAID-induced gut injury.

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Notable Supporting Compounds (Honorable Mentions)

• Curcumin: Potent anti-inflammatory, downregulates hepcidin and supports iron regulation, reduces heavy metal burden, may mitigate some pain.
• Chamomile: Used for pain management in endometriosis.
• Boswellia: Sometimes combined with quercetin & curcumin for extra anti-inflammatory action.

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Timestamps for Key Segments

| Segment/Theme | Timestamps | |------------------------------------------|----------------------| | Introduction & prevalence | 00:00 – 12:07 | | Understanding endo—symptoms, physiology | 06:17 – 11:26 | | Common medical treatments | 04:01 – 12:07 | | Dysbiosis, bacteria, histamine | 12:07 – 21:16 | | Beta-caryophyllene & TA-1 | 22:20 – 26:14 | | Diet (FODMAP) intervention | 26:43 – 29:09 | | Microbiome, estrogen detox, probiotics | 32:36 – 41:37 | | Antioxidant defenses | 41:55 – 47:55 | | NAC for endo | 48:51 – 54:29 | | Melatonin and pain | 54:29 – 57:07 | | Pycnogenol | 58:06 – 62:26 | | Heavy metals/mod. citrus pectin | 62:34 – 70:17 | | Iron, lactoferrin, supplementation | 70:53 – 76:21 | | Pain: PEA, NSAIDs, practical tips | 77:13 – 80:34 | | Conclusion | 82:20 – end |

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Memorable Quotes

• “If someone has just been diagnosed with endo… what are some of the things you could implement immediately that are probably going to be the most bang for buck?” — Jake [03:05]
• “There's almost this positive feedback loop of estrogen–histamine–inflammation that just compounds the issue.” — Dave [16:40]
• “The most potent antioxidants are the ones you produce… look after melatonin and glutathione first.”
  — Dave [44:50]
• “24 of 47 women scheduled for laparoscopy canceled after NAC.” — Jake, on a pivotal clinical NAC study [57:07]
• “MCP (modified citrus pectin) is the best fiber powder by a mile for this”; “If we’re having a shootout between PHGG and MCP, MCP wins, hands down.” — Dave [70:25]
• “PEA is not just about pain—it also protects the gut from NSAID injury.” — Jake [79:47]

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Final Notes

• Not all interventions discussed are widely available or inexpensive (e.g., TA-1, Beta-caryophyllene, MCP).
• Many approaches overlap and address multiple endo drivers: pain, hormone regulation, inflammation, and gut health.
• The podcast’s tone is friendly, conversational, and encouraging; both hosts share client stories, scientific references, and pragmatic tips.

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Takeaway

This episode provides a robust, practical springboard for anyone seeking to manage endometriosis beyond the conventional toolkit. From the microbiome to mitochondria, the hosts deliver research-backed and clinically nuanced methods that can be considered alongside or as complements to standard medical therapy.

Transcript

[A]

Welcome back. Thank you for joining us for a gut feeling. Now, Dave, I haven't told you this, but we had a request this week to do a live event in Newcastle and I had to break it to the people. I told them that we were meant to do one and you bailed on us and I threw you under the bus.

[B]

Well, well, there's. There's a lot to that story. Okay. Like, obviously we're not. We're not. We're not going to tell the entire story on a podcast. Okay. But, you know. You know, it's not as simple. It's not as simple as I bailed on the.

[A]

I know, but the people that didn't know that it made a better story. But what I. The point here is I thought I would tell you on air so you can't back out of it, that I told everyone we will be doing an event when you come back.

[B]

Well, we're definitely going to do a live event. Yeah.

[A]

Okay. In Newcastle.

[B]

In Newcastle, yeah.

[A]

Okay, great. Now that I've got a public commitment, we can.

[B]

That's the end of the podcast.

[A]

That's the podcast done. I hope you join us again next week for another episode of Gut Feeling. So our episode today is a little bit different. Who knows how it's going to go? I never know how any of it.

[B]

Like, just before, just before you get into it. Okay. Because, like, you. You, like, you're going to tell a bit of a story here. Okay. And.

[A]

Okay. Building me up.

[B]

But would you say this is almost like we're doing like a bit of a case study? It's probably like.

[A]

Yeah, sort of.

[B]

This would probably be the first case study that we've actually done on a podcast.

[A]

But anyway, it's a vague case study. Okay. Because a lot of people are going to see themselves in this case. We're not going to be going super specific, like, oh, you've got this blood marker and you got this and that, or whatever. So what we're going to talk about is.

[B]

Probably could do that. Yeah.

[A]

But, you know, it's an interesting idea. We could do that in the future. Yeah. I don't know if people would find that interesting or not. So what we wanted to do is talk about a condition that has been getting a little bit of attention online at the moment, and that's endometriosis. And without.

[B]

Well, to be honest, I keep on interrupting you.

[A]

Okay.

[B]

By the way. But I. Well, until you told me this story. Okay. Which I'm sure the listeners are really looking forward to, this story, I wasn't

[A]

going to tell this story because I don't want to, like, name names. So now you're putting me in an awkward position, but, yeah, you can do it.

[B]

Well, sorry. Sorry to throw you under the bus, okay. But I didn't even know this was a big story again till you actually told me, you know, told me what was going. Told me what was going on. Okay. But anyway, I'm gonna, I'm gonna leave you to it.

[A]

So we could have had plausible deniability, but now because you've accused me of this, now I have to tell one. So. Okay, here we go. I don't like naming names. I don't wanna. We're not, we're not sort of putting anyone down here, but for some of you guys, I'm sure you follow Brian Johnson online. He's sort of a renowned biohacker and his partner's been diagnosed with endometriosis. And they're doing a lot of work documenting this experience and documenting the diagnosis and talking about what the treatment's going to be. And there's been a lot of, a lot of people talking about this, a lot of, you know, people asking questions, hey, what are you going to do? What's the treatment going to be like? All this kind of, you know, I guess around this, this issue. And it made me think if, if I was diagnosed with endo, which, you know, that'd be an unfortunate thing. And you know what, endo can occur in men as well, but obviously super, super uncommon. But it made me think, if I was diagnosed with endo, what are the things that I would be reaching for, first of all, to help. Yeah. Without spending, like, I know that, you know, they're trying to document this whole experience and whatever, documenting millions of different biomarkers and biometrics during Kate's period and all this stuff and like, all power to them, collecting data. But if someone has just been diagnosed with endo, and, you know, we know that often this takes years of, you know, pain and sort of confusion before people actually do land a diagnosis. Well, what are some of the things you could do, you could implement immediately that are probably going to be the most bang for buck and potentially going to help your quality of life significantly?

[B]

Well, we should say that most people. Okay, they're. You would say, I mean, I don't think they call it this. Okay. But it'd be sort of like a three prong approach to trying to deal with it. Yeah. Okay. Now obviously there would, there would be the obvious here. Okay. Which would be laparoscopic Surgery. Okay. So going down the path of surgery.

[A]

Okay.

[B]

Then there would be like hormonal suppression, like therapy and then usually it'd be

[A]

the pill or IUD or something like that.

[B]

Exactly. Yeah. Okay. And then there'd be like pain management. Okay. And more than not. Okay. When we're talking about pain management, it's really probably going to be like NSAIDs again, like non steroidal anti inflammatory drugs. Okay.

[A]

The more severe the pain is and they might even end up using things like endone and, and more potent painkillers as well.

[B]

Yeah. So like, like opioids, basically. Yeah. Okay.

[A]

Yeah.

[B]

I don't, I don't think they really, they don't go to, they don't go, they don't go down the path of using like. Yeah, like morphine or something like that. Okay. But. And obviously using. And obviously using. Yeah, obviously using things like Panol and paracetamol. Paracetamol and all that type of stuff.

[A]

Well, for a lot of people with Endo, it's not going to particularly touch. Like that would be the, you know, very starting point and it probably won't do a whole lot. So, you know, often people do end up using pretty significant painkillers.

[B]

Yeah. And obviously, like, you know, one thing that I would mention. Okay. Is that, I mean, do we need to. I mean, I think most people probably. Do most people know what endometriosis is? I mean, do we, do we like. Obviously we like to give like some, you know, context. Well, a bit of context, a bit of a definition of what it is. Okay. But do we need to do that?

[A]

Yeah, I mean, I guess a little bit. I don't want to get too caught up in it.

[B]

And don't worry, I'll try and keep it as simple as possible.

[A]

Well, part of the purpose of this episode as well is we're not going to go. I know you're going to want to. We're not going to go super, super deep into the physiology and the biochemistry of this. Yeah, we want to. Because I don't know if you said it yet, but we want to introduce 10 interventions you could look at. And so obviously 10 is quite a few. So I'm gonna, I'm gonna contain you or constrain you and not let you go too deep into it. But let's, let's start with a little bit of a working definition. What are we talking about when we talk about.

[B]

Well, I'll try and keep it as simple as possible. Yeah. Okay. Because like, obviously this would be where there's like there's patches of tissue that grow in other areas of the body that are similar to. To the lining of the uterus. Yeah, okay. Yeah.

[A]

And so endometrial, like, tissue is how they would normally. Yeah.

[B]

And in research, a lot of the time they call, like, endometriosis, like, implants. Okay. That's what they call it. Yeah. Okay. And, you know, and the thing, like, more than not, I couldn't give, like, percentages around this. Maybe you could. Okay. But more than not, that sort of, like, tissue growth. And obviously one of the biggest drivers, okay. Around tissue growth is going to be estrogen. Yeah. Okay. Hence why, obviously, the link with, like, Eastern dominance and so forth. But once again, what is causing the estrogen dominance? And that's obviously a big conversation, but the, A lot of time, okay. The areas that you. That someone would develop by endometriosis, okay. Would be like, the. The ovaries, like, the outer surface of the uterus, even, like, fallopian tubes, I think, like the ligaments of the uterus, even. I can't remember what this is called. I think there's a particular name for it, again, where it can be, like, the deep space between uterus and the rectum and so forth. But I mean, some people can get, like, the. They actually develop by endometriosis. We were talking about this, like, just before we jumped on, again, where people can get it in, like, areas like the appendix. Okay. Obviously within the digestive system as well within the bowel and the bladder. Okay. I, I think I was mentioning to you that some people can get it in the thoracic. Now, I'm not saying that's a high percentage of people. Okay. And they've actually got, like, different names for that type of, like, endometriosis. Okay. But people can get it, like, in the thoracic cavity. Okay. Like, you know, the chest and the lungs. Okay. I guess my point is, okay, that you can get that tissue growth in many different areas around the. Around the body. That's my point. Yeah, yeah.

[A]

And it is quite a complex condition, obviously. And you've mentioned how estrogen plays into it. And then we're going to talk a little bit more in a moment about how potentially there's an impact or an influence or things like bacterial issues that are influencing estrogen and how that's actually being regulated. And. And, you know, we even know that there's, you know, other issues around. Like, for example, we'll talk a little bit later on about, you know, potentially like, iron overload in tissue. And so there's there's quite a bit going on and there's a bit of debate over, like, is this a, is it like even autoimmune sort of properties or sort of characteristics when it comes to Endo? Is it predominantly a hormonal thing? First and foremost, like, it's quite a complex condition. And by all, by no means is this going to be a, you know, completely kind of comprehensive podcast on endo. We want this to be sort of, hey, this is something you're dealing with really actionable things. You can start to think about, you can start to implement. You know, it's, you know, we're both aware that this is such a life changing condition for a lot of people. And, you know, I've worked with plenty of women with ENDO who, you know, they're bedridden for a week every month. And you know, I mean, what are,

[B]

what are the, what are the. I mean, it was a while ago that I looked at these stats. Okay. But I mean, I think of women of like, reproductive age. Okay. This would be like, I think like, globally, isn't it something like, what, like 190 million women or something like that? Okay. I think it's like, isn't it in the, like, it's getting close to sort of like, like 10%. Yeah. So when I say 10%, I'm obviously talking about 10% of, of women of reproductive age. Yeah. Okay, so. But obviously we're talking about, you know, pretty high numbers.

[A]

Yeah, yeah, it's, it is, it does seem like it's more prevalent. Hey, like, you know, you talk to people and everyone knows someone nowadays who's got endo.

[B]

You know, it's, I don't, I don't, I don't know how much has actually increased over the. Cause I actually haven't looked at those stats. That would be interesting to understand how much it's actually increased over like, you know, sort of like the decades. Okay. Yeah, I'm not sure around that. Okay. But I'm sure there has been a steady increase. Yeah.

[A]

I would say with the people I've worked with, women who have Endo, they're almost, I'm trying to think now, like, I would say they almost seem to be the most grateful when there's a change in symptoms. Like, you know, I've had a number of women who've gone from, like I said, being bedridden, you know, five, six, seven days a month. And then, you know, maybe they, you know, don't need any painkillers. I've had several where they don't need any painkillers anymore. Maybe they need painkillers for one day a month now instead of, you know, being bedridden for a week. And the change that that has on people's lives is astronomical. You know, like the, like, I can think of a couple of clients at the top of my head who, like, periodically message me, and they're just like, I can't believe, like, that I'm not stuck in pain every month. Like, every time I get my period, I think of you, and they send me a message, and it's like, this is. This must be such a debilitating sort of, you know, state for so many people. It must take such a big toll on people's quality of life.

[B]

Well, it's. It's. It's also. It's. It's also nice to know, okay, that when someone is. When someone is not in a lot of pain, the first person that they think of is Jake Doshu.

[A]

Anyway, it's a funny one because it's easy to become accustomed to new baseline. You know, so it is interesting that I do notice with. With women with endo, when they do see their pain diminish, they actually take. Take note of it instead of just taking for granted. So, you know, obviously, I think that speaks to how. How much of an impact that's having on their life, you know, so let's jump into it. You sort of said, hey, conventionally, people are going to look at pain management, they're going to look at hormonal suppression, they're going to look at surgery. We're going to kind of categorize the. Our interventions into those sort of categories. Do we want to go with that order? Do we want to start with pain? Maybe we take a step back and we start with the hormonal side of things. Is that a good place to start?

[B]

Maybe, like, in terms of the. The sort of, like, like talking about the issue and dominance.

[A]

Yeah. And. And what might be influencing or impacting some of these hormonal issues. Right. So obviously just going on birth control or IUD or whatever, like, that's not a solution. That's not a fix for endometriosis.

[B]

Well, like, well, even like. Okay, so, you know, I think we don't need to go into this into a lot of depth, because I think we've actually covered this in a completely separate po. Okay. So I think if people track down the podcast that was actually on histamine. Okay, they would be able to listen to this. Okay. But it's also the relationship that histamine has. With estrogen. Yeah, okay. But then once again, what's actually driving up the histamine? But basically, we know that actually, basically histamine, okay? So if someone does have, you know, high amounts of histamine, okay? And we obviously know that bacteria is a big driver behind that, okay? But histamine is. Increases estrogen production, okay? And then also in regards to estrogen, okay. Which is actually to do with, like, you know, mast cell receptors, okay? So mast cells are a type of immune cell, okay? But mast cells are to do with histamine, okay? But basically estrogen actually upregulates the expression of histamine receptors, okay? So they're protein molecules. And so that was like H2 and H3 receptors, the histamine receptors, okay. And that would actually cause a higher synthesis and release of histamine, okay? And so what happens here, okay, is that people just get stuck in this. They get stuck in this sort of loop, okay? Now I would generally say some of the biggest culprits to drive up the histamine, okay? Well, one is sibo, okay. And we actually know one of the byproducts from SIBO is histamine. Okay, I'll touch on this one a little bit more. Okay. And because like, most SIBO is made up of negative gram bacteria strains. Or you like to say gram negative. That is actually the correct terminology.

[A]

Okay. Everyone else likes to say gram negative,

[B]

as you know, okay?

[A]

The.

[B]

So it's. It's generally made up of, you know, klepsin, ammonia, estrogen, E. Coli bacteroids, okay? Yeah. And we actually know that there's obviously an enzyme called histidine decarboxylase, okay. And basically that enzyme converts dietary histidine to histamine, so it ramps up the histamine. And we know that like, negative gram bacteria strains, gram negative, okay. They have higher activity levels of that enzyme. And that's actually been documented, documented in a lot of like, negative gram bacteria strains, okay. Like, things like, you know, Klepsa, aerogenes, Morgan, Morganella, Megani, Hafnir, Alvi, Citrobacter fundi complex, you know, Pseudomonas strains, okay? You know, a lot of. A lot of negative gram bacteria strains, okay. And even we know with like, lps, and we're going to touch on LPS a lot more, okay? So lipopolysaccharides. But one thing I want to make, make, make clear is LPS is not always the devil, okay? There's obviously, you know, certain types of LPS can actually help with Immune parameters in children can actually help with ASP cells. You barely recognize foreign antigens, foreign material. Okay. Obviously, there's a certain type of LPS that we're talking about here, like hexa acylate or hexacylation. And like, when they've done research around, like, you know, like LPS, when they've administered LPS, it actually upregulates, basically, H1 receptors. Okay. So the histamine receptors. And in that research, it actually created, like, rashes and hives and. And so forth. Yeah. Okay. But, yeah, like.

[A]

So the big point here is that.

[B]

Well, one. One thing I just wanted to. Sorry. One thing I just want to mention around that. Okay. Is. And also we do know, okay. Like, histamine is derived from things like uterine odarin, like epithelial mast cells. Okay. And you get, like, when you've got elevated estrogen levels during the menstrual cycle, induces, like, histamine release. Okay. And I think we've spoken about this in the past where, you know that. Where they looked at, like, allergies, okay. In regards to, like, histamine, and they actually showed that that was more prevalent in women with hormonal imbalances such as, like, endometriosis, like within that research.

[A]

Yeah. Because you're getting that. That sort of loop of estrogen and histamine. Yeah, yeah.

[B]

And there's also, like. They've looked at things like plasma, like estradiol and progesterone concentrations, and they. They showed that they actually correlated with clinical symptoms around, like, asthma, which is ultimately like a histamine issue. Yeah. Okay.

[A]

So anyway, so there's almost like this positive feedback loop that's occurring where you've got this, the estrogen, sorry, the histamine and inflammation and even like, up regulation, even in things like crusty glandins. And then that's increasing aromatase activity, that's increasing estrogen even more. And so it just kind of becomes this. This. Yeah. Positive feedback loop that just increases this issue over time. Yeah. And you're saying that, you know, this issue around potentially negative gram bacteria or gram negative bacteria is driving a lot of this. And there's more and more research coming out around this as well. Like, especially over the last few years. I think this May, maybe about 10 years ago or so, I think there was a paper published called. I think it was called endometriosis, the bacterial hypothesis, maybe 10 years or so ago. But then since then, there's been a whole lot more coming out around sort of connections to different microbiome. And bacteria.

[B]

Sorry to interrupt, but it's like, look, it was a while ago, but haven't they shown that they. In some literature that in regards to like endometriosis that they, some of these individuals may have larger, larger numbers of like beta glucuronidase producing bacteria?

[A]

Yeah, and there's, there's also research showing that women with endo had more LPs in the menstrual blood as well. So this is not like, you know, I know that study called it a hypothesis and you know, sure. What's underpinning or you know, what's actually behind the pathophysiology of endo? You know, that's maybe a bigger question, but I think it's. It's pretty safe to say that the E is a highly prevalent of these bacterial issues and dysbiosis and gram negative bacterial issues.

[B]

Well, I know. Yeah, sorry. Sorry to interrupt again. Okay. But I know they bear in mind, okay, this was a rat model. Okay. So a marine model. Okay. But they, they were looking at aspects around. And this is even the conversation around like oxative stress and persistent oxative stress. And we know that LPS is a big driver behind that. Okay. But they actually showed that the like LPS induced like pelvic inflammation. Okay. And then it basically because it induced like the pelvic inflammation, enhanced like the development of like endometriosis like lesions. Okay. And because LPS just ramps up all these pro inflammatory proteins. Like even. So one would be like NF kappa B, which is being linked to like accelerated aging and things like you know, ra, rheumatoid arthritis and. Okay. But basically like LPS will ramp up these prime family proteins like NF kappa B. Anyway, sorry to interrupt. I just wanted to add that.

[A]

Yeah, yeah. So what would be some interventions that would target this side of things, target the bacterial side dysbiosis, the histamine inflammation, the, the estrogen sort of loop. What might we suggest there to start with?

[B]

Okay, so we. Are we linking this in with the LPS scenario or we. Yes, yeah, yeah.

[A]

Because it's sort of all part and parcel, really.

[B]

Yeah, yeah, yeah. So. So, well, one thing, like, I'm not saying this is fully going to rectify it. Okay. But just based on this sort of like histamine estrogen loop. Okay. Well you'd think anything on that is gonna also even just stabilize mast cell activity. Okay. Would have some huge benefits and like we don't need to go into a lot of depth around that. Okay. But that could be like, you know, quercetin which is a biflavinoid flavonoid. Again, that's really good around stabilizing mast cell activity, but also a pa. And isn't that interesting because, like, PA is probably one of the best compounds around pain management anyway.

[A]

Yeah.

[B]

Okay. Which is obviously palmitoid lethanolamide. Okay. It's a fatty substance. Okay. It's an endocannabinoid. We produce it. But you also do get it from, you know, egg yolks and peanuts. Okay. But we covered this in the most recent podcast that we did. Okay. It doesn't mean you're going to sit there and eat a whole heap of egg yolks and you're going to solve that problem. Yeah. Okay. So I would look at things that would stabilize the mast cell activity. Okay. But also even things that would be pretty good at, like, binding to lps. Okay. Well, actually, lactoferrin's pretty good around that. Okay. Binds to lps, it destabilize negative ground bacteria strains. I think we're going to mention lactoferrin again, okay. And there obviously there can be some like, you know, Tyras gel, which is a silica based compound. But anyway, okay, I would be looking at.

[A]

You're suggesting all the things we said we weren't going to suggest.

[B]

What.

[A]

What here would you use for LPS specifically?

[B]

Okay. All right. So now, interesting myth is, okay, I've. I've done a fair bit of research around. They're called, like, tollite receptors, okay. And there's one called, like, tolerant receptor 4. One thing I do want to mention, okay, because you mentioned these things, and then people just think these things are all bad, okay, like tolerant receptors, they're mediators, okay? So they're basically just like a class of proteins. They play a key role in the innate immune system. My big point is, what, they're normal, okay? But one of their key roles, okay, is to recognize, like, molecules that are derived from microbes, okay? And there's certain things that can really ramp up toll, like receptors, and in particular toll, like receptor 4, okay? And toll, like receptor 4, has been linked to things like breast cancer and lung cancer and sarcomas, like bone cancers, all that type of stuff, okay? And so when it's. I'm talking about when it's chronic and prolonged, okay, they can reach the liver through the portal blood, and they basically activate inflammatory pathways within the liver. Basically. Okay? Now if you actually look at some of the research around this, okay, They've actually shown that it was in regards to toll, like receptor 4. Okay. But that was significantly overexpressed, okay. In the endometrial tissue and the lesions or patients with endometriosis. Okay. So what they actually, I think it was separate research, okay. Where they actually looked at pharmacological. I can't remember what compound they were using. Okay. But they did a pharmalogical inhibition of toll like receptor 4. Okay. And what it was actually shown to do was reduce lesion growth. So what that concluded is is supporting around like toll like receptor 4, using something like a inhibition for that. Okay. Could be a pretty promising non hormonal therapeutic target around the endometriosis. And now my big thing would be. Okay, and there was actually like a 2017 study where they actually showed there was the activation of toll like receptor 4 by LPS. Okay. So from my perspective, one of the biggest culprits to ramp up toll like receptor 4 is LPS. So, okay, now we can use compounds to target Toll like receptor. To target Toll like receptors. Okay. And target things like toll like receptor 4. I think I mentioned. Mentioned this to you. Okay. One that's pretty interesting around this, okay. Would be TA1, which is thymosid alpha 1. Okay. Obviously it's a peptide. It's 28amino acids. Okay. But without going too, because obviously we've spoken about

[A]

peptides.

[B]

Yeah, yeah, okay. Like TA1 Thymus and Alpha 1 targets tall like receptors. So that's sort of like pretty interesting around that. Okay, but then, okay, what, what do I believe are some of the most significant compounds, okay. Around the actual lps, okay. Now one that I'm really big on, as you know. Okay. But I do acknowledge there can be a bit of murkiness around. Like, okay, what would be the ideal dose? Because when you look at there, there is human subjects when it comes to this compounds beta cariflame, which is terpene. Okay, so there are human subjects, okay. But I think that was to do with like cigarette smoke, okay. Where they, they, they basically were using it to deal with things like passive smoking and all that type of stuff. Anyway, whole separate conversation, okay? But this was. The beta caraffene was to do with like endometriosis implants. And I've already mentioned that. Okay, this is obviously where there's patches of tissue that grow in other areas around the body that would have a similar lining. Similar. That would be similar to the lining of the uterus, basically. And so they use beta caraffine, okay. That was shown to suppress the growth of the endometriosis implants by 52.5% that was compared to the controls in adult female rats. But once again, it becomes a bit of a conversation. Okay, what's going to be the ideal dose? Okay. Because obviously, obviously you've got to try and do the conversion. That's easier said than done. And so. Okay, but they also show beta carophylline is really good around oxative stress and persistent oxidative stress. That's going to be something else that we're going to break down. Okay. But the beta carafeline induce apoptosis, which is basically like getting rid of cells that have sort of like changed beyond repair. Okay. That was in the luminal epithelium of the ovarian endometrioma, basically. Okay. Now my big point is, okay, because I say this to people and they go, also betacaraphylline just really amazing around like women's health ailments and okay, it's really great around like endometriosis. Now my, my thing would be no, Beta Caroline is really great around one of the major culprits to why the person has endometriosis, okay. Because beta carrefin has been shown to reduce the abundance of proteobacteria, okay. That is negative gram bacteria, okay. And even batty caraffine. Okay. There was once again, it's mice, okay. But they were pre treated with like batty caraffine. Okay. And they'll actually, they were actually shown, it was actually shown to reduce, okay, the production of low pro inflammatory proteins, okay. So things like Interleukin 6 TNF Alpha, Interleukin 1 Beta, okay. There was a 50% reduction in those pro inflammatory proteins, okay. And a lot of those pro inflammatory proteins, they're raised up by LPS. Yeah. Anyway,

[A]

yeah, so, so you mentioned TA1 Thames now for one and beta caroflam. Now you touched on sort of a few kind of bits and pieces. Then one other thing we, you obviously, you talked about antioxidants. We'll talk about that in a moment. But you sort of mentioned you were talking about lactoferrin actually helping bind to, to lipopolysaccharides. Yeah. To lps. Now lactoferrin, so that's a glycoprotein. So it's found in like in milk and. Well, I guess milk's probably going to be the main source where people can get away.

[B]

We talked about like camel milk is crazy high in it. Okay, but I understand.

[A]

Which most people aren't including in their diet, to be honest. But we've told you that. But you know, from a dietary perspective. Again, we'll talk about lactoferrin more in a moment. But interestingly, dairy is a funny one because anecdotally, some people, and you see this a lot in, like, the. The natural kind of, you know, neutropathy kind of world where people will say, oh, if you have endo, you shouldn't consume dairy. Right. I'm sure you've heard people talking about that. Now, what's interesting with that is there's not really, as far as I'm aware, any research to support that. And in fact, there's several studies that actually show that a high dairy intake is associated with lower endometriosis risk. Now, obviously, that's just an association. It doesn't prove causation. But I do find that interesting that, in fact, the opposite seems to be true. Dairy doesn't seem to be an issue, and it does make me wonder about things like lactoferrin. But sort of besides that point, from a dietary perspective, I think one that's really well documented is a lower fodmap diet. And this is especially true if you look at the studies on women. So women with endo are far more likely to have IBS symptoms. Right. And obviously some of that might just be due to, you know, pelvic inflammation and kind of what's going on with the endo itself. But then some of that is going to be due to what you said there. As far as the dysbiosis goes. Now, we're not going to stand here and say, hey, low FODMAP is going to fix dysbiosis. It's. It's not a viable treatment per se, but it certainly is a viable symptom management tool.

[B]

Well, the whole thing would be that you're just not flaming the fire. Okay. Or you're not adding logs to the fire. Okay, Whatever. Whatever analogy you want to go with.

[A]

Yeah, totally.

[B]

Yeah.

[A]

Yeah. And, you know, if someone's at a point where, you know, they're experiencing excruciating pain and symptoms, I think that is an easy intervention to give a go. You know, like, I get that limiting diet is a bit of a pain. No one loves to do it, but there's so much stuff out there now that's low fodmap. It's not that hard to trial a low FODMAP diet. I think it makes sense as an intervention to give it a go at least for a few months while you're doing some of these other things, especially if you're adding in some of These things that could be helping with dysbiosis as well. Then hopefully you'll get to a point where you can introduce back in some of those FODMAP foods.

[B]

You know what, you know what I mentioned? You know what would be an interesting like, like I'm, I'm not saying that I've done this, but it would be sort of like an interesting experiment. Like maybe we will do this maybe.

[A]

Okay.

[B]

But it'd be interesting, it would be interesting to see like, okay, you know how like there can be certain types of like biomarkers and blood markers that might give you like some insight. Okay. To maybe the presence of some like endometriosis. Now I'm not because I think a lot of time don't they check like a thing called like CA125 levels? Okay.

[A]

Yeah. What I've seen the data that's best is probably the neutrophil to lymphocyte ratio.

[B]

Oh, okay. That's interesting. Yeah. Okay. But yeah, I, I, I, I think I read some stuff around they looking at like CA120 levels, which is like measuring protein in the blood. Okay. Which is, I think it's like cancer antigen 1, 2, 5 or something like that. Okay. And they generally say that the levels should like, I think they should be less than 35 units per millimeter or something like that. Okay. But without looking at that. Okay. You know another marker where I think there, there is some supportive literature around. Okay. Can actually be like ESA erythrocyte sedimentation. Right. Okay. Which is obviously the rate at which the red blood cell sediment within a given hour. Now most of the time in medical realms they're looking at that around like ongoing disease severity. Okay. For things like lupus and maybe rheumatica and ra, you know, polymylgia, all that type of stuff. Okay. But you can definitely look at ESR around things like mycobacterium bacterial and fungal, which is basically just like CO infection, like multi layered bacterial issues. And also like auto, like auto. It can be a sign of like auto antibodies. They've reacted with gut bacteria. Okay. And this would be aspects around like molecular mimicry, molecular mimics and so forth. Okay. But my thing, okay. Would be okay if they have actually shown that, I think that and that I'm pretty sure they have shown this like ISR levels that increase. Okay. That can be sort of like a representation of like endometriosis severity. Well, okay. You know, could CO infection, multi layer bacterial issues. A lot of time that would also ramp up the esr. Yeah. Okay. Anyway, I think it'd be a. Interesting experiment. Okay. To see if, you know, there's a bit of a correlation here. Okay. With certain markers that would be off skewed by some of these underlying bacterial complications and gut issues that we're talking about.

[A]

I mean, the same could be said. I mentioned neutrophils and to lymphocyte ratio a moment ago. The same could be said of that. You know, if it's dysbiosis and bacterial issues, then it wouldn't be shocking to see a higher neutrophil, you know, count there as well. So I wouldn't be surprised at all. As far as LPS, so we've now covered TA1 beta carathalin. I'm putting low FODMAP diet into that sort of category as well. One that maybe is worth mentioning. And it sort of fits into a couple of sort of sections. But I don't know. I don't think you've mentioned it in too much detail, but obviously one of the issues with the. The estrogenic component of endometriosis is there's. Without wanting to go into too much detail here, part of the way that, that hormones are detoxified essentially is, I guess, bacteria dependent. Right. And so we can have bacteria usually in large intestine, which can actually be producing an enzyme called beta glucuronidase, and that actually leads to reabsorption of. Of estrogen. Right. And so bacteria is involved in both, I guess you could say, the mismanagement as far as, like hormonal detoxification goes, but then also facilitating some of that. That sort of detoxification as well.

[B]

Because obviously we're talking about there is the estrogen. Yeah. Okay. And the estrobolom is a collective of bacteria. There's a bit of like, like how many strains really make up the estrogen. I've read documentation where they say it's like 60 different strains of bacteria. Some of those strains can be actually, like pathogenic in nature as well. Okay. Which really is just more evidence around, you know, microbiome homeostasis. Okay. Making sure you don't have gut dysbiosis. Okay. Which is unbalanced gut microbiota. Okay. But the, the issue of balm, okay. Should be. Should predominantly be within the colon, large intestine. Okay. And so the, and, and that's made up of like, you know, bacterial strains like even, like enterococcus and even like Escherchia coli, like all these different types of bacterial strains. And so what the Ischobolum does, okay? It modulates like the interior hepatic circulation of estrogens, okay. Basically, so we're talking about like a modulation and regulation process here, okay? So the, the microbes in the estrobolum, okay, they produce, like you've said, okay, like an enzyme, a protein molecule called beta glucuronidase, okay? And so the beta glucuronidase, when you have like conjugate or bound estrogen, okay? So the, what you're going to do with the, the bound of the conjugated estrogen, okay, is you're generally going to eliminate that. You're going to clear it, and most of the time you're going to clear it by, you know, urine and feces, okay? Now one of the roles of the, the estrobolom in the beta glucuronase, okay, is to take the conjugate or the boundation unconjugated, which is a technical word for what, unbind it, okay? And then you're going to. So now you have more activation, okay? So basically that enzyme, it dec. Conjugates the estrogens into the active form. This is a modulation process, okay? And so now you have more activation now with the help of like other gut bacteria like Lactobacillus. So that's why they basically say Lactobacillus is a carrier for isshin. So it actually helped to. So it actually helps to sort of like recirculate each and back through the bloodstream. Again, once again, modulation, okay? But obviously what can happen here, okay, is that you can have high amounts of the issue bolum within the small intestine. Within the small intestine. So areas like the duodenum, you know, jejunum, ilium, okay? Then you have. So you've got high. So that could, obviously this could be gas exchange issue, motility issue. You're struggling with like high fermentable food indigestible matter. I mean, the poster child of all gut dysbiosis, okay, conditions would be sibo, small intestinal bacterial overgrowth, okay? And then you can have high amounts of ischobolum that are making up your sibo. They're producing more of the beta glucuronase, okay? They're taking the conjugation, they're unconjugating it. You have more activation and that can obviously lead to the issue dominance. Anyway, I got there. Yeah.

[A]

Well, something else interesting actually that you made me think of when you're saying that is that enzyme beta glucuronidase so obviously that's largely present in the large intestine. The effect that's going to have on unconjugating the estrogen part of that is going to be time dependent. Right. So the longer that the estrogens actually depend, I guess present with the beta glucuronidase is going to influence how much that becomes unconjugated. And so impaired motility, slowed motility, let's say constipation will ultimately exacerbate that. And so SIBO obviously is one of the main drivers behind constipation, really. So that becomes another one of those loops where, okay, you've got this dysbiosis state anyway, that's leading to more beta glucuronidase, that slower motility is leading to more of an effect of that beta glucuronidase. And again, this stuff just. It just all compounds over time, doesn't it?

[B]

Yeah. And also when you've got eastern dominance. Okay. You weaken the pelvic floor even more.

[A]

Okay.

[B]

Which might actually lead to like, more frequent urination potentially as well. Okay. But also you're delaying gastric empty. Okay. So then you just like get more constipation. And then also estrogen has a relationship with your thyroid. Okay. And you can increase things like tbg, like thyroid binding globulin. Okay. And then that binds to free T3, which is the more bioavailable thyroid hormone. Okay. Which now you might get sluggish thyroid, you know, hypothyroidism, Hashimoto's. And the thing is, when you generally have sluggish thyroid and hypothyroidism, you're a lot more prone to what? Constipation. I mean, like, I mean, we could talk about so many loops here.

[A]

Yeah, yeah, absolutely. So there's a few things that can influence beta gluconidase and conjugation. And, you know, people often will talk about calcium D glucarate and that's an option. And you know, I use that with clients sometimes. But one that can modulate some of this and what we're talking about here with the bacterial issues and the estrobolom. Well, probiotics can actually have a role to play here. And it's a tricky one, I guess, where the question's always going to be like, well, which probiotics? You know, does it have to be a particular strain? Sort of. Do. Do most probiotics do similar things? And I would say that I don't know how you feel about this. I think it's maybe not super, super clear. Like, I think we've got a good idea, some that may be potentially more effective than others. Maybe. But, you know, I. Arguably, if you took a step back and you looked at probiotics as a whole, you could probably make a case for a lot of different types of probiotics that could be beneficial here. Whether it's stuff like spore based organisms that are going to help reduce polysaccharides entering the bloodstream, whether it's stuff like Saccharomyces bolati, which is going to have almost like an antimicrobial effect against some of the pathogenic opportunistic organisms, whether it's stuff like. You probably want to talk about Lactobacillus and Lactobacillus gastrii, but there's a whole lot of different options here that I think could potentially have merit. Now, I would say there's not a whole heap of research when it comes to different probiotics and endometriosis. There's a little bit of data out there. So there was one study published a few years ago where they did use, I think it was a Lactobacillus sort of combination probiotic, and that did lead to significant reduction in symptom severity. And that was in pain. They looked at different types of pain and pain across the board all dropped quite significantly. So it is definitely one that I think is worth looking at. Is it going to be. Would that be the top of your list as far as endo supplements?

[B]

Not really. I mean, like, like, I think I've looked at some stuff. I don't know how conclusive this is either. Okay. Like, you know, because, you know, how much does just like dysposis of the vaginal region. Okay. Play a role in this? Okay. You know, I don't know. Yeah. Okay. I couldn't really give it. I couldn't really give a percentage amount of. Because obviously, like, I would say when it comes to bacteria. Okay. I would say females are a lot more simpler within that. Within the reproductive organ region. I'm not talking about the structure of the reproductive organs. I'm just talking about the bacteria. Does that make sense? Yeah, the microbiome. Okay. Because they're just meant to have like a lot of Lactobacillus strains within that region and then that decreases the ph balance. Okay. Which actually, that actually protects them around things like Gardnerella and so don't get a fishy odor to the, the vaginal region after sex and oriental stuff. Yeah. So. Yeah. Like how much, like, you know, dysposis of the vaginal region. Okay. And so one of the bacterial strains, okay. That is quite dominant. Okay. Within that region is Lactobacillus gasseri. I think there's some stuff around it sort of suppressing like ectotopic tissue growth. Okay. Which sort of like that, that would actually drive. Which actually that sort of drives like the, like it's an estrogen driven process. Yeah. Okay. And so, I mean you could definitely find some, you know, research around that. Okay. But I guess what you're asking much of a needle mover is that. Okay. I mean, it wouldn't like. Yeah. To answer your question, it wouldn't be one of the things that I'm just going, you've got to do a. You got to take like a Lactobacillus gasseri. Okay. I wonder, I wonder like, you know, people might go down the path of suppositories. Okay. But have you really looked into that? I mean, I haven't looked into that.

[A]

I don't know that there's any research on it. I do think it'll be interesting because, you know, again, if you look at things like UTIs. Well, the data on probiotics and UTIs is okay, but the data on probiotic suppositories and UTIS is better. And I wouldn't be surprised if you end up finding that with endo as well. I just don't know that it's been studied.

[B]

Yeah.

[A]

So. Yeah, potentially. And, and you know, it may even be the thing where both are effective. Right. Because you know, I mentioned LPS in the blood of, of immenses. Blood of people who have endo. And the question there is, well, is that LPS is coming from vaginal microbiome and it may well be right. But then we also know that there's this despotic state which is common in the gut as well. So maybe it is a. Actually an oral probiotic and the suppository may actually be the best approach there, but we just don't have that data.

[B]

We might be, we might be onto something there, mate.

[A]

It's. I'm hoping that suppository pro bodies become easier to access because I do use them with clients somewhat regularly and they're just fairly hard to actually come by.

[B]

Hard to come by. And sometimes they don't always have like the best breakdown with the suppositories as well. So anyway, let's. There could be a bit of a niche for anybody listening.

[A]

Anyone listening, making probiotics. Yeah. So. Okay, well, we're about halfway through our list now. So we've covered low FODMAP, TA1, beta carathylene probiotics. Not quite halfway. We've done four of 10. Should we move on to antioxidants? That's a big category.

[B]

Yeah. Well, even around the. The case study that you sort of, like, brought up. I do, I do. Like, how much have I looked into the stuff around, like, Brian Johnson? Like, have you looked. Have you. Have you looked into a lot of the stuff in terms of what he's really big on? Okay.

[A]

I must say I'm relatively Adrian to a lot of his supplements. I've seen a couple with when clients have taken them in past. What I would say. I don't know if you've seen this. He does like, a cacao supplement. Have you seen that?

[B]

I haven't seen it.

[A]

It's actually. It looks quite solid. I considered ordering some myself. I couldn't. I don't think there's anywhere in Australia that sold it. But the cacao supplement does look quite good.

[B]

But, but do you tend to find, I guess, the. The path that I'm going down? Okay. Do you tend to find that especially, like, a lot of these longevity people and all that stuff? There's just this huge focus on this whole thing of, like, you know, the mitochondria and the cells and.

[A]

Yeah. Okay.

[B]

And also, like, oxidative stress. It's all about oxative stress. Okay.

[A]

Yeah.

[B]

You know, persistent oxide stress. And I'm. Look, I'm not saying these aren't factors. There's no doubt that oxidative stress, again, drives endometriosis. Absolutely.

[A]

Yeah. We're not arguing against that.

[B]

Yeah, we're not arguing that at all. Okay. I mean, like, there's pretty good documentation around, like, worsening, like, pelvic pain and all that type of stuff. But I guess the question mark here is. Okay, but that's all well and good. Okay. But then people have this perception that oxidative stress is all bad as well. Yeah. Okay. And so obviously the conversation is like, you've got free radicals. Okay. And basically with, like, the big issue here would be persistent oxidative stress when it's sort of, like, you know, prolonged. It's ongoing. Okay. That's a big issue. Okay. But oxidative stress, okay, is where you have too many free radicals. But then people think free radicals are all bad. Okay. But they're just unchanged molecules. Okay. But free radicals, they are pretty essential. They're like essential players even in your innate immune system. So we're Talking about, like, initial response. So you're going to produce free radicals in many things, like the metabolism of food. Okay.

[A]

Breathing.

[B]

But most people just focus around the liver because obviously the liver produces free radicals in regards to detoxification. But white blood cells will basically send free radicals to do what? Destroy bacteria and viruses and, like, damaged cells and all that type of stuff. Because. So I just wanna make it clear, though, it doesn't mean free radicals are the devil here. Does it make sense? Okay, so they say the fifth. The. Obviously, the aspect around oxidative stress is when you have too many free radicals and you don't have enough antioxidants to neutralize the free radicals. But then I think a lot of people think that really has to be, like, there's gotta be a high amount of, like, phytonutrients and fennels, and it's gotta be like, you know, green smoothies and juice cleansers and all that type of stuff. Okay. But let's be honest here. When we talk about the most powerful, powerful antioxidants. Okay. It's the antioxidants that we produce.

[A]

Yeah. Yeah, that's fair.

[B]

Melatonin.

[A]

Yeah.

[B]

Okay. Like, that is. Well, can we safely say it's probably the most powerful antioxidant in the human body?

[A]

Well, I mean, look, the two that people are going to fight over will be melatonin and glutathione. And I mean, we're going to talk about both of those.

[B]

Yeah. So you got melatonin cholesterol is a powerful antioxidant. Again, that's kicking. That gets completely demonized. Okay. And then you've got glutathione. Okay. They call it the master antioxidant. But really the reason it's a master antioxidant because it actually helps you to recycle other antioxidants being like, vitamin E and vitamin C. And doesn't, like, Dr. Brian Walsh say that they're probably the only true free radical scavenger. Okay. Is vitamin E. Okay. And what they say that 86% of people don't hit the recommended daily ounce for, like, vitamin E? I don't know if that's true, but. Okay, let's say it could be a pretty high percentage. Okay. And so that's why glutathione is so important. Yeah. Okay. So I would say these are the most powerful antioxidants in the human body. Okay. And could we say that a lot of people might have issues around, like, melatonin and glutathione? I Mean, definitely those two. Okay. Maybe we get into a bit of debate around the cholesterol scenario. Okay. But I guess you understand my point. Okay. I don't like. But also, we need to look at what is driving the persistent oxative stress. Okay. And based on what we've already talked about, one of the biggest drivers for persistent oxidative stress is metabolites and byproducts coming from bacteria.

[A]

Yeah.

[B]

So you can throw all these things.

[A]

We started with that section, to be honest.

[B]

Exactly. Okay. We know, like, go, go look at the research. Lps. Okay. Drives persistent oxative stress. Like, you, you, you. You'll find that easily. Yeah. Okay. And so the thing is, you can throw all these things at the mitochondria in the cells and. Okay. Like, but if you're not stemming the flow. Yeah, okay, like, that's a big issue. Okay. I'm just seeing quite the people, just this hyper focus. Okay. On what do I need for the mitochondria and the cells. Okay. I think they're sort of like, they're missing what antioxidants are really important here. Okay. Because we know this. The most potent and the most powerful compounds. Okay. That actually help us to deal with a lot of these things are the compounds that we produce internally. That's what you've got it. That's what you got to look after anyway. That's probably like a podcast topic in itself. Yeah.

[A]

Yeah, true. I mean, we could do a whole topic on. On antioxidants as a whole, to be honest. Like, I think that's such a misunderstood topic. But either way. So we're not saying don't look at using antioxidants. We're saying that that's probably not the only piece of the puzzle, and you need to be asking why is it so.

[B]

But also, like, a lot of some of the compounds we've already mentioned. Okay, well, I mentioned that, you know, beta caroflam.

[A]

Yeah.

[B]

I mean, beta carafine is amazing around, like, mitigating, like, you know, persistent oxative stress and oxidative stress. Okay. So my point is, okay, even the stuff around, like, you know, quercetin. Yeah. A lot of the compounds we've already mentioned. Okay. They're very good around that.

[A]

Okay, so you're already on our list. I guess that's our bonus 11th one by the time you finish. Because, like, quercetin is certainly. It's one that I often do use with people who have endometriosis. And like, you're saying it's covering antioxidant properties, you know, it's got some antimicrobial properties. It's obviously helping as far as the gut lining goes. And it's. There's good data on it. Right. Like there was, there was, I think it was a fairly newly published, like a review article on, on all the potential mechanisms of quercetin when it comes to endometriosis. And you know, they're talking about anti proliferative effects. There's anti fibrotic effects of curcumin, obviously the antioxidant effects, anti inflammatory effects. So it's, it really is very multifaceted when it comes to endo.

[B]

Yeah, but I know, I know there's probably a compound that you want to touch on quite a fair bit when it comes to the oxidative stress and the persistent oxidative stress. I don't know. Blake, do you want, do you want to talk about. You know what?

[A]

I think it's worth starting with nac because we've just covered the dysposis sort of side of things and NAC kind of bridges that gap really well. Yeah. Because you would usually use NAC with dysposis.

[B]

Well. Because obviously we're talking about like precursor to glutathione. There you go.

[A]

This is an antimuculyic as well. Right. So obviously it's going to help with biofilm. So if you are doing any sort of, you know, disposal kind of treatment, using any antimicrobials,

[B]

it basically disperses and it thins out the biofilm. Okay. It's really good around like bacterial virulence factors. I mean, we've spoken about that in previous podcasts. Okay. So it's, it's got like anti quorum sensing properties as well. Okay. And obviously, you know, you've got L cysteine. Okay. Which is sulfur based amino acid. Again, NAC is a supplemental form of like L cysteine. Okay. So N acetyl cysteine. And you look at something like NAC that can actually help to revive. Okay. Like glutathione as well. Okay. So you sort of say like a precursor to glutathione. Okay. And I guess that's sort of like the part that you're going down. Okay. In terms of.

[A]

Well, how often would you say, you mentioned blood work before and you talked about sort of bloods you might see with endo. I feel like I can't sort of point to any data on this, but I feel like the girls I work with who have endo, high prevalence of low ggt. Right. Is that, is that something you feel like you've noticed at all?

[B]

I mean, I bet you if I really put a laser attention on it. Okay. I would imagine that would probably. That would probably be the case. And I think we've spoken about this. I mean, obviously this was like, you know, my studies. Okay. But they basically showed that mice that actually had a cysteine deficiency. Okay. They actually had a lowering in ggt. Okay. And there is some stuff around, like, really bad overburdening in the. The gut to liver access as well. Like driving down the GGT as well. Okay. And you'd probably say, like, LPS is. Is a huge culprit around that. Okay. Because like, LPS just catabolize your glutathione pools. That's what it does. Yeah. Okay. So, yeah, probably a couple of factors. Okay. To why that would, like, you know, drive down the, you know, the ggt. Yeah.

[A]

So nac, we've actually got good data on NAC when it comes to endo. You know, it's been shown to reduce endometrioma size. It's been shown to reduce pain or improve pain, reduce inflammation. It's been shown to help with fertility outcomes in women with endo. There's even one study, I think it was an Italian study. Do you know this one, where they had women who were scheduled for laparoscopy and they were given nac. And I forget how many it was. Like, there were many women. I'll have to send you this. This is so funny. So I think it's about 20 women scheduled for laparoscopy given NAC. It was NAC three times daily. I forget how long this study was for, but almost all the women who were given NAC ended up canceling the laparoscopy because, like, obviously just to do improvements, Right? Like, the NAC helped that much. I'm pretty sure it was something like 18 of the 20 women. Something along those lines. I need to double check it. But it was. It was. Majority of the women ended up canceling the laparoscopy. So nac, I think, is one of the most underrated endo supplements. It is. People can look up that study. In fact, in a moment, I'll pull it up and I'll give the exact numbers over that because I don't want to misquote it, but I think nac, really, for me, that's one of the first supplements I reach for when it comes to endo. Now, do you have an opinion here? So this is one I don't think we've actually talked about. This. When it comes to nac, some people do, like, daily dosing. They take every single day for weeks or months. Some people do, like, a cycle where they take it half a week on, half a week off. Do you have preferred way of dosing

[B]

NAC when it comes to ENDO to do with endometriosis? Yeah.

[A]

Yeah.

[B]

I mean, but I mean, like, have you seen, like. I can't remember the dosage again, but I think it was, like. Because obviously there's documentation around things like oxidative stress and persistent oxidative stress where people were, like, driving up the amount of, like, the nac, like, really high.

[A]

Okay.

[B]

I. I think you've talked about some of this research, and that was obviously in, like, elderly participants. I think it was.

[A]

Yeah. Yeah.

[B]

Weren't they driving it up around about, like, getting, like, anywhere between 3,000 to 5,000 milligrams?

[A]

Yeah, it was about that at 4,000 on average. Something like that. Yeah.

[B]

And I. I think I've come across stuff, okay, where people are even taking, like, 2,000 milligrams, which some people might think is a pretty high dose. I don't think that's a very high dose. Okay. Doing, like, 2,000 milligrams. And that's just for, like, inflammation. Okay. Just to mitigate information. Information. They're sort of, like, taking that for, like, 36 months.

[A]

Yeah.

[B]

Okay. So that's like, I'm at six. Telling people to do that. Okay. But I'm saying that's. That's like three years. Okay. Doing that. So, like, look, my point of view is that, like, some people. Now, obviously, some people can have issues with nac. This is a different conversation. Okay. They can have, obviously, like, you know, sulfur metabolization issues and underlying, like, you know, polymorphisms and gene defects where there might be a bit of a problem with the nac. But from my perspective, okay, I think people can take, like, NAC for quite extended periods of time. Okay. I don't know if that's.

[A]

You would just do it daily, then you wouldn't do, like, a half week on, half week off.

[B]

I would tend to do, like. Like, daily. Yeah.

[A]

Yeah. I do both with my clients. And it depends maybe on, like, how long I plan on using it for. The only reason I do sometimes cycle it is because some of the studies in endo, they. They did a cycle. And so I'm not convinced that that's necessarily better. But I do often just like to kind of match what they.

[B]

This.

[A]

If a study has really good findings, I kind of like to match what the study did. But I think you could probably make an argument either way. So nac, definitely one of the most effective antioxidants there. Should we talk about melatonin? You brought it up a few times.

[B]

Yeah, I mean, look, to be honest, I haven't, you might have looked into this a little bit more than me. Okay. Like, I haven't directly looked at the, the research papers around like melatonin with like endometriosis. Okay. But there's no doubt. Okay. That melatonin is one that, you know, I've already mentioned it. Okay. It's one of the most powerful, you know, if not the most powerful antioxidant going around. Okay. And so, you know, we, we, we obviously know that melatonin can be a big problem for a lot of individuals. So you would think in regards to something like endometriosis, like melatonin could be a bit of a no brainer. So I don't know if you've looked at the.

[A]

There's, there is mixed findings on melatonin. I still think it's quite good. There's certainly some good animal studies. There's one where I think they used 10, this is a human study. I think they used 10 milligrams, which is, you know, obviously that's a relatively high dose of melatonin. And I think there was like a, almost a 40% reduction in pain scores. So there certainly is compelling human research. And in that same study they noted that painkiller use was, you know, significantly reduced in the women using the melatonin. And we'll talk about pain in a moment. But obviously this is one thing there that could help with pain. So, so yeah, I, I definitely think. And again if you look at the animal research, it's really compelling data there around actually reducing the, the lesion growth as well or reducing lesion size, which, you know, that's. Anything that, that's been shown to reduce lesion size I think we should be paying attention to. So melatonin is one that I would, I would usually use with a lot of my endo clients. Yeah.

[B]

That like, did you say, did you say that the um, like just around like the, the, the dose amount that a lot of time is sort of like recommended within the research.

[A]

Yeah. So that human study was 10 milligrams. Okay.

[B]

Which like, isn't that really interesting though, okay. That you say that now that I'm thinking about because like I would generally say when people have like LPS issues because melatonin. Okay. Is great around like LPS issues. Okay. Because we know that LPS can actually damage the blood brain barrier outside the blood brain barrier, and that obviously puts a lot of pressure on melatonin. Okay. Because actually, melatonin is really important for the function. For the function of the. The tight junction proteins in the blood brain barrier. Okay. So things like occluding codum 5 and. But generally you need to go quite high with the melatonin dose. Yeah. Okay. I think a lot of doc. Some of the documentation might be around that sort of like 10 milligram mark. Okay. So I do that. I do find that pretty interesting. That is, they're sort of having to drive up the. The melatonin dose to actually have those. Those benefits. And is that just, like, more proof of this underlying sort of like, LPS issue?

[A]

Yeah, yeah, potentially. Hey, and I do think you can make the argument, like, 10 milligrams, while that is a high dose, if you were just using it for sleep, I don't think it's an excessively high dose as, like, an antioxidant supplement. And I, I do think you could probably argue, hey, maybe even trying, you know, push out to 20 milligrams. There may well be some merit to that as well, potentially. I found that NAC study I was referring to a moment ago. I thought I'd just quickly read out the results of that. So 24 of 47 women canceled their laparoscopy. So that was in women using nac. And in the control group, there was only one woman who canceled the Prescott. So just over half, which is, you know, that's pretty good. Pretty good numbers, really, considering that's a monotherapy. They didn't do anything else. And they were using 1800 milligrams a day. And again, that was only half week on, half week off. So pretty cool. And it was only 12 weeks, which is not that long. Okay, now antioxidants was there. Oh, there was another one we were going to talk about.

[B]

Well, do you want to, like, obviously one of your favorites again, do you want to talk about just the stuff around, like, French maritime pine bark extract, which is like.

[A]

Yeah, I mean, look, this probably is. I would say. I mean, it's got to be in my top five favorite supplements. And it just helps with so many different things. Right. And obviously this isn't a podcast on. I say pycnogenic. What do you say, Pete? Nodginal. I don't even know. Yeah, I mean, like, as Australians, I think we're meant to put the emphasis on the first vowel is that how it goes?

[B]

Most likely. Most likely.

[A]

I don't know.

[B]

I mean, Australians don't always have the best, you know, pronunciation of things.

[A]

Well, I tend to pronounce stuff like Americans do and I always get told off for it. But, you know, obviously people tend. There tends to be more American based sort of alternative health educators anyway, however you're meant to say it. Pycnogenol. That's what I'm gonna say. Obviously. I think, I think we've talked about it as far as some of the like, cognitive effects did. We did. We did. I think ADHD podcast, I think.

[B]

I think we've also just talked about in regards to things like, you know, muscular endurance and muscular capacity and I mean, even. I even just like some of the stuff around blood flow. Yeah, okay. Because obviously it's pretty good for like Enos. Okay. Which is like endothelium, not endothelial, nitric oxide, which is enzyme. Again, that's, you know, winding the blood vessels and. And okay, so vasodilation. And so I think there's, you know, there's been many instances that we've actually where it's mentioned. Like picnogenol.

[A]

Yeah, yeah. I mean, you know, there's stuff around, especially neurological symptoms is obviously amazing. Like there was one study that found similar efficacy to Ritalin in kids with adhd. You know, if you look at even stuff around like skin issues and stuff like cellulite, lipedema, pycnol can help with that. Obviously you talked about the performance stuff. Dysmenorrhe. Whole lot of research around dysmenorrhea. But there is also research around endo and it's one of those ones where it's graduated on a whole lot of pain issues. So there's even studies in like the third trimester of pregnancy and helping with, with back pain. And, you know, it's a supplement I would use as someone if they just had like joint pain or back pain or, you know, anything like that. And so the question becomes like, is it helping here as far as like, pain goes? Is it helping with inflammation? Is it mainly helping as an antioxidant? Obviously it's a very potent antioxidant, but in women. And you talked about at the start how like hormonal treatment is, you know, one of the avenues for endo. Well, there was one study where they had women who were taking. It was just like birth control, basically some hormonal treatment with endo. And some of them, half of them were given pycnogenol. On top of their contraception. And in those who were given pycnogenol, around 50% of them had complete elimination of pain in 12 weeks. And as far as recall was that,

[B]

was that the same research? I mean, I'm sure there's a few research papers, but was that the same research where they were just talking about like minimizing like you know, heavier periods and more painful periods and even aspects around spotting and bleeding and all that?

[A]

Yeah, potentially. Yeah. I think it might have been men.

[B]

Yeah.

[A]

And in, in the contraception only group, there was zero women who had complete elimination of pain. So like, you know, to go from 50% to zero just by adding in the pycinol and they didn't even do, I would say they didn't do a massively high dose. So they did one 20 milligrams a day. So 60 milligrams twice a day. Which like that's, you know, it's decent, but it's, it's not like excessively high by any means.

[B]

Well, I mean is the reason that we say it's decent because obviously some like Pycnogenol is just quite an expensive compound.

[A]

It's an expensive supplement.

[B]

Yeah, I think it's more, more to do with that. Okay. Because you, you probably. Because a lot of time they're sort of talking about anywhere between 100 to 200 milligrams, something like that. Okay. But I wouldn't say the amount is excessive. Okay. Far from it. Okay. I think it's just a case that's pretty expensive. Expensive.

[A]

Yeah, yeah, yeah, yeah. You know, I often, I would do like 150 with my clients. I think, you know, if you can afford it, 200 milligrams. Like there's other studies showing benefit in other conditions at those higher doses. But you know, like you're saying it is a fairly expensive supplement.

[B]

I'm losing track of all the, the, of all the different topics. Okay.

[A]

That we, I think we're almost there, so. Wow.

[B]

Actually. Okay. Well, I think there's, there's definitely the, like just some of the, the links between endometriosis and like even like heavy metals. I, I don't think we've done that.

[A]

Well this, this, I think two that fall into that category. Hey, so yeah, let's do that. Let's cover.

[B]

Well, I don't want to.

[A]

ICOs.

[B]

Well. Cause I've. Well, let's start with just like, like heavy metals. Okay. Because I've actually looked into some of the, the research papers around this and they. They actually looked at. They're looking at like blood concentrations. Okay. Of obviously, like. Like heavy metals. I think, like, within that research. Okay. It might have been they're looking at certain heavy metals individually, but then they were looking at combined exposure of those heavy metals. Hopefully. That makes sense. Okay. So they'll. I think they're looking at things like arsenic, cadmium, lead, mercury. I do actually find the. The a little bit interesting around like cadmium, lead and mercury more so probably cadmium. Okay. Because they do tend to make up biofilm. Yeah. Okay. Because obviously certain types of bacterial. Australians have an affinity for certain types of heavy metals. I generally say very established, very robust biofilm. A lot of time can be made up of like, cadmium and lead. Okay. But they basically showed that even like, like, just like individually. Okay. Or even as a. Like a mixture. Okay. There was a risk of like, endometriosis. Yeah. Okay. And I've looked at some. They actually, like, just in regards to cadmium. Okay. Because obviously cadmium can actually cause. Which you get from like, like brain pad fumes. Yeah. Okay. And they. And cadmium can actually cause like, demineralization of bone as well. Again. But they had women, okay. That actually they had the highest, like, blood levels of cadmium. Okay. And I think it was cadmium and lead actually. Okay. And they were three times more likely, okay. To have like endometriosis can, obviously, compared to the women that actually had the lower. Lower. Had the lowest. Lowest levels of the lower, lower levels. Even aspects around like, mercury. What was it? Something like 13 times more common in women. Okay. Even like, I think it was like arsenic, it was like five times more common. So there's obviously a bit of a link here. Okay. And we would say that probably the best compound. That's probably going to cover many bases. Okay. To deal with this. Not probably. It is the best. Okay. Would be, well, ultimately integropectin if you could find it. Okay. But your. You're not going to find it. I think there's a place in Italy that's got the patent on that. But you got integropectin, which is like organic lemon waste and the rind, all type of stuff. But then you got like, Then you got mcp, okay. Which is modified citrapectin. Okay. Now you know my thoughts, okay. I think this is the OG of all fiber powders. Okay. I think a lot of people would push back on me in regards to that. But. But I am convinced, okay. It is the best fiber powder from my perspective, that is My viewpoint by my. By mile. Okay. And when they've done, actually, and this actually is the good thing about some, like integrate pectin, modified citrupectin. It covers the bacterial aspects as well. Okay. Because I did research around, like lemon integra, lemon integral pectin, okay. And actually, because modified cincipectin, integral pectin is very high in terpenes, like kempferol, that actually stops cell division in cancer cells. Okay. But they compared lemon integropectin, concentrated hydrogen peroxide, which is like a nuclear bond to bacteria that was in regards to E. Coli. Yeah. Okay. And actually showed that the lemon integropectin created twice as much oxative stress within the E. Coli than the concentration than the concentrated hydrogen peroxide. Even around, like, Staphagogsaurus, which is obviously like, so antibiotic resistant, drug resistant, okay. Like 88.82% resistance rate against like penicillin, for example. Okay. They. They were looking at the more pathogenic, the more virulent forms of staphylococcusaurus, okay. And they actually showed that the integropectin had significant antimicrobial activity against the staphylococcusaurus. Okay. But obviously the big thing is around, like, heavy metals, okay. 74% reduction heavy metals, okay. Mainly around cadmium, lead and arsenic, I think. Okay. There's obviously the stuff around, like, children in China where they gave, like, a tablespoon, which is. Is pretty high dose, okay. For like, young children, okay. A tablespoon of modified citrupectin. It was very well tolerated, no adverse events. And even if you look at what. What are the. What, like, if there are any adverse events or symptoms, okay. I think a bit of minor diarrhea potentially. Okay. And that it basically dealt with the lead, okay. In that research, okay. And that was in young children. Okay. So, but the good thing about mcp, okay, as a GI binder, okay. It doesn't bind to any minerals. That's why you can have it close. Okay. It doesn't bind to things like selenium, zinc, magnesium, iron, calcium. Okay. Was one I missed there. Okay. Anyway, so. But a lot of people, okay, I think they start going down this path of, like, GI binders, okay. Where they've gone zeolite or bentonite, clay or anything like that. Okay. And obviously these things, okay. Well, they do bind to these trace minerals and minerals that I'm talking about. Yeah.

[A]

Well, I don't know that many people would be thinking about binaries in the context of endo at all, you know, When I use modifiers, he's just packing. With people, people, it's always one where they're like, what's that? You know, they've never heard of it. And I don't think they're. You know, I don't see people taking charcoal or taking zero light or stuff for this either. And it is. It's. It's. I would say of the supplements we're talking about, obviously you've talked about stuff like Beta Caroline, TA1, you know, stuff that is super kind of niche and maybe harder to source. But as far as, like, the category of supplements you're talking about, I would say this is the most overlooked hooked when it comes to endosupps. Like, not only does it do all the stuff you've just said there as far as heavy metals, but it's also super valuable because it actually inhibits something called Galactin 3, which is what? Signaling molecule involved in development of endometriosis lesions. Right. And also like PCOS as well. A whole lot of other chronic inflammatory diseases and conditions, too. So it's potentially even having an.

[B]

Bear in mind, okay, some pretty amazing stuff around batty caraffrin with pcos, but I won't go down that rabbit hole.

[A]

Yeah. But in a different mechanism, though, I think this is really interesting because there's not a lot that actually inhibits Galactin 3, especially from a natural kind of, you know, standpoint.

[B]

Well, I think you've told me. Okay. Like, that actually. They've actually shown that Galectin 3, apart from obviously being overexpressed in things like, you know, colorectal cancer, colon cancer, and all that type of stuff. Yeah, but you've told me it's been actually overexpressed in things like traumas. Like, and that would be like, you know, things like emotional traumas and childhood traumas and all that type of stuff. And we know Galactin three causes, like, cognitive impairment, it as well. Yeah. Okay. Anyway, sorry. Sorry to interrupt. Okay. But don't you think the whole thing with, like. Anyway, this is just my thoughts around it. Okay, but don't you think there can be. I feel like the reason that MCP is not on a lot of people's radar. Okay. Maybe they look. They just haven't looked into it a lot. Okay, but don't you think it's a case of they sort of like, weigh things. They weigh things up based on price? Price. There you go.

[A]

To an extent. Yeah, definitely. When it comes to fibers, I do think that's the case. And, you know, that's for me. That's why I don't use this more. I would love to use it more, but it is. It is a really expensive fiber, and so I have to reserve it for when I think someone really needs it. And typically that is a heavy metals issue or an endo issue.

[B]

But you know me, if I had my way, it just should be, like. It just should be the go to. Okay. When it comes to fiber powers.

[A]

Okay.

[B]

I just think, like, if we. I've told you this before, if we're having a shootout between, like, phgg and like, modified citrapectin. Modified citrapectin, from my perspective, wins. Hands down. Hands down. Okay. Anyway, that's. That's, that's. That's my viewpoint. Yeah.

[A]

I do still like Pheg, I must admit, for. Especially for C. Worm and BE Fan. Okay. Metals. So that's where we were. Let's talk about.

[B]

I think we've covered that base, haven't we?

[A]

Yeah, I think we've covered metals, but let's talk about iron. So iron, you know, sort of adjacent. And iron's a funny one because a lot of women with endo, you would. You would think have low iron. And they do. Right. Like, that's a common issue when it comes to endo because obviously there tends to be heavier bleeding and, you know, blood loss with menses. And so women are more susceptible to low iron. Iron, you know, iron requirement is. Is much higher in women than it is men. And obviously most women aren't eating as much iron, so, you know, that becomes a significant problem. And, And a lot of women with endo are then told to have iron supplementation.

[B]

Well, it's crazy.

[A]

Yeah. Well, yeah, I mean, you know, we laugh about that, but people might be a bit confused as to why that's an issue if they're listening to this and like. Well, hang on. If people are low in iron, doesn't that make sense? So what's.

[B]

Well, they're actually shown. And if you look at the research, okay, they've shown that iron itself might contribute to the migration abilities. Okay.

[A]

Of.

[B]

I mean, they're looking at, like, endometriotic cells. Yeah. Okay. And. And, and if females, like, if they end up going down that path, okay. Of where they're doing, like, you know, you know, iron infusions. Okay. Inorganic organic iron supplementation. Okay. The problem here is, okay, there's a possibility of getting, like, secondary iron overload.

[A]

Yeah.

[B]

Okay. We obviously know that iron is highly toxic in the body. Okay. But you get iron overload and then what it does, it compromises the ability of phagocytes, which is neutrophils and monocytes, predominantly neutrophils, okay? To basically kill microorganisms, okay? So now you increase the survival of certain type of. Certain types of bacterial strains, like yersinii and vibrio, okay? And you're a lot more prone to. To dysbiosis, okay? Which is basically unbalanced gut microbiome, okay? And when they've done research around, like, chronic overload, okay? Now obviously this was in, like, thalassemic patients, okay? But they actually showed, okay, that there was impaired innate immunity, okay? And there was a manipulation of lysozymal function, okay? And so lysosome is amp antimicrobial peptide. And you need lysozyme to help with, like, panacell recovery, restore panic cell function, rescue panacells. And from my perspective, the. To mitigate gut dysbiosis is penicills. Okay? So then you're. Now you've just got more dysbiosis. That's my point. And also, like, are we really looking into what might be leading to even things like iron accumulation, all that type of stuff? Okay, now we've been speaking about LPS quite a fair bit. And is there documentation of lps? Because obviously LPS induce, like, look, it's one of the worst culprits to ramp up, like, pro inflammatory protein proteins, okay? So it induces inflammation, okay? But then also iron accumulation at the tissue level, okay? So then if you get, like, antipaside, which is like, fat cells, okay, you get antipocyte inflammation. It disrupts iron homeostasis, okay? And then you get, like, antipaside, like, iron overload. So the thing here would be like, this is even. There's even, like, overlap in terms of this topic, okay, with the LPS scenario again. Yeah, yeah, yeah. That's my point. Yeah.

[A]

Well, you know, one thing you didn't even mention there is you're on the hepcidin as well. Yeah. So you ramp up inflammation, you have dysbiosis, LPS ramps up inflammation, ramps up something called hepcidin, so a hormone. And one of the functions of hepcidin is it essentially reduces iron absorption, but it also basically traps iron inside cells and tissue. So now you've got this state where there's potentially, you know, lowered kind of digestive absorption of IR iron. Maybe someone's more prone to iron deficiency, but you actually have these dysregulated, you know, imbalanced iron when it comes to tissue Levels and tissue iron accumulation. And you see this with endo.

[B]

Yeah.

[A]

You see, you know, endometriotic lesions. You know, commonly there's iron accumulation within that tissue and surrounding tissue. So to just say, oh, well, you know, you're low in iron because you've got endo. Here, take this iron supplement. It's like, well, you could be making things worse.

[B]

And then on top of that. Okay. They're probably. We go, oh, we'll be careful with something like curcumin. Okay. Just.

[A]

Oh.

[B]

Because that might actually inhibit the, you know, the. The uptake of the iron. Okay. Where we would actually look at it. Okay. Because obviously, like, the hepcide is ramped up by. By prom puncture cytokines like interleukin 6. Viral infections, bacterial infections. Okay. And what's one of the best compounds to actually, actually inhibit hepcidin? Curcumin. Okay. So anyway, it's a whole other conversation.

[A]

Yeah. And metals as well. We've been talking about heavy metals. And curcumin's quite good around heavy metals too. Yeah, yeah. And curcumin is not even on our list, but it is. Would be one that I would certainly consider with someone who's got endo. So what would be. We've talked about iron. What would be a supplement that one could consider if they're not going to use an iron supplement?

[B]

Well, I think we sort of already. Yeah. Mentioned this before. Well, lactoferrin. Yeah, okay. Lactoferrin. And now I've already mentioned. Okay. Because at least with the lactoferrin, you're tackling the LPS scenario as well. Okay. If I'm saying it destabilized negative ground bacteria strains. Okay. It binds to lps. I mean, you're covering way more bases than that. Okay. And even if it's to do with the structure of the gut lining. Okay. Where there must be compromisation in that. Okay. Because obviously, like, lactoferrin helps with, like, enterocyte growth. Enterocyte cell proliferation. Okay. So now we're even talking about, like, improving aspects around assimilation, absorption, all that type of stuff as well.

[A]

Yeah, yeah. And the cool thing with. With lactoferrin, as far as iron goes, is it's. It's not an iron supplement. Like. Yes. Okay. Lactoferrin is partially saturated in a small amount of iron, not a huge amount amount. The main way that it's working, though, is around the hepcid. It's helping reduce inflammation, it's helping modulate iron absorption. So you're kind of Getting this benefit as far as iron levels and iron status goes without taking an iron supplement.

[B]

Yeah.

[A]

Okay, where are we? I think we've done. We've got one, one more pain. Pain is our last category. And look, we've talked so many of

[B]

the supplements we talked about, but clearly we didn't.

[A]

Indirectly. We have, yeah. We've talked about pycnol. We've talked about, you know, NAC helping with pain. We've talked about melatonin helping with pain. So, so many things we've talked about indirectly will help with pain.

[B]

But even, even like, like, even though, even though they're not renowned for it. Okay. I mean, a lot of, like, you know, curcumin. Yeah, okay. You know, like beta carafine's got benefits around pain as well. Do you know what I mean?

[A]

Yeah. So all these things will still help. So, you know, and that's why, you know, we've only got one thing in this case category because all this other stuff has it covered. But we needed to include this, and that's pea. And you've mentioned PEA a moment ago. I forget you were talking about eggs. I don't know how it came up, but pea.

[B]

Well, it's really good around like a thing called ppar. Okay. Which is to do with like inflammatory, you know, like inflammatory properties in terms of mitigating, like, you know, information. Again, obviously there's pretty good stuff around, like neuropathic patients pain, they come in. What is it like, you know, 10% of individuals, I think, based on the U.S. experience like neuropathic pain. There's, there's stuff around like, what's the prevalence of things like headaches and migraine with aura and recurring headaches in like, endometriosis? I couldn't tell you, but I would imagine it's a symptom. Yeah. Okay. And so there's, there's just the stuff around that as well. Okay. We know that PEA is really good for like a migraine with aura, recurring headaches. I mean, there's this stuff around the severe headaches. I mean, obviously we've spoken about that in the past.

[A]

Yeah, yeah, yeah. And just from as far as, you know, pain goes when it comes to endo, you know that this is another one of those supplements where there's actually research on Endo and it's been shown to reduce endometriosis related pain, reduce pelvic pain, dysmenorrhea pain, painful intercourse, even painful like bowel movements as well. So it is one of those ones. It's more than Just symptom management, but it's also kind of symptom management management. You know, if I had anyone with a chronic painful, you know, pain condition, I would be adding PEA initially just to help improve quality of life. But, you know, obviously it's having all these other effects as well. It's helping with function, it's helping with, you know, even, even, you know, the gut lining. What's interesting here actually is you mentioned the stuff.

[B]

A bit of a side note. Could we have a. Let's not go down this rabbit hole because I'm opening a can of worms here. Gaba, could we have a strong conversation around someone like GHKCU as well with endo? Yeah,

[A]

anyway, yeah, well, it is a rabbit hole because, you know, the. Yeah, let's not, let's not. But pea. What was I going to say with that? Nsaids, you said, hey, you know, a lot of women with endo, they're going to be taking NSAIDs or paracetamol or, you know, some kind of painkiller. And we know that a lot of these painkillers have a detrimental effect on gut lining. You know, they, they cause permeability. Whether that's permeability.

[B]

The worst thing is they downregulate ecad air and expression.

[A]

I mean, there's a lot of worse things in there. I mean, look at the effect of glutathione as well, you know, so there's a whole lot of things that are going on. But what's interesting with PA is these direct studies where they take it alongside NSAIDs, and that mitigates the actual permeability caused by the NSAID. So if someone's taking NSAIDs, my first choice would be by taking PA instead, if it's not enough for you. And you know, I understand not everyone responds as well to PA as they might NSAIDs, it depends on the person. But then I'd say, well, can we reduce that NSAID dose and supplement it with pea? And at least you're going to mitigate the damage of that NSAID. Yeah, so that's it. That's our 10/question of 11.

[B]

That was a bit of a, bit

[A]

of a beast, bit of a whirlwind, I will admit. But, you know, there's a lot there. And like, to be, to be honest, that list we've talked about. Yes, there's a couple other things I use with clients and we've mentioned curcumin and I use inflamed gut. So that's Kirkman quercet in Boswellia. What else might I use? I use chamomile because that can help significantly with pain as well. But, you know, there's not a lot else. Like, that's pretty much my full endo protocol that covers just, you know, every single base really you can think of, you know, and is. Is there anything there we've said that's going to be an issue for some people? Like, sure, everyone. Every now and then someone might have a weird symptom to something, but none of that is. Is that specialized.

[B]

Yeah, but I think we start getting in the weeds of conversations around, like, people go, well, mcp. Oh, that's expensive. But that's. This is, this is like a, like that's. It doesn't. Like, it's. It's such a. It's such a good fiber powder. It's such a good, you know, supplemental intervention. Okay. But I mean, now we're getting to the weeds of the price.

[A]

Yeah, yeah. Cost. But, you know, that doesn't mean that it's. It's going to be dangerous for some people. You know, like everything we've said there, like, it's, it's all fairly well even.

[B]

I'm a huge fan of it. I'm a huge fan of Buddy Caravan. Definitely, like around something like endometriosis and women's health ailments. But now we're just getting a conversation with people go, oh, it's hard to find. But that's just a different conversation. Does that make sense? Okay, so.

[A]

Well, actually, I know a supplement company that sell it. They call the Collective Supplement Code. What is that? What is that product called?

[B]

Got to Brine Access Blend.

[A]

I collect the supplement code. So if you are looking to be careful, as far as I'm aware, that's the only commercial product for Beta Cariflames.

[B]

Very, very, very, very hard to find. Very hard to find. Yeah.

[A]

So I think that's our episode done. Is anything. Anything you want to finish with?

[B]

Well, I think we've been pretty thorough there. You know, maybe like not fully a case study, but maybe our sort of first sort of case study scenario.

[A]

I mean, look, let us know if you like this. If you're one of the four people who made it an hour and a half in. Let us know if you want us for, you know, something else.

[B]

Pcos or forward it to Brian Johnson.

[A]

Yeah. Maybe to Kate. I don't know. Maybe. Yeah. Let us know if this was helpful. Let us know we can do it again. If no one made it this far, then that's okay. We won't do it again. Okay. Thank you, guys for tuning in. We hope you'll join us again next week for another episode.

[B]

Thanks, guys.