Andrew: As we do tend to chat.

Beth: We do.

Andrew: Today, Beth, we’re gonna be talking about beta-glucuronidase, calprotectin, zonulin through these sort of descriptive markers. So I guess to start, can you take us through what each of these are, please?

Beth: Yes, absolutely. Well, if we start with calprotectin, calprotectin is a protein released by neutrophils. So when there is inflammation in the gut GI tract, neutrophils will move to the area, release calprotectin resulting in an increased level in the stool. And so, fecal calprotectin is a way to detect inflammation in the intestines. We know that intestinal inflammation is associated with inflammatory bowel diseases such as Crohn’s and ulcerative colitis, and some bacterial GI infections. So calprotectin can be used to help distinguish between inflammatory bowel diseases and non-inflammatory conditions such as irritable bowel or IBS.

Zonulin is a marker of intestinal barrier integrity of, more specifically, the small intestine. So, again, it is a protein produced by intestinal and liver cells, and it reversibly regulates intestinal permeability by regulating the tight junctions between the cells of the GI tract. And this was discovered back in 2000 by Dr Alessio Fasano and his team at University of Maryland. And they called it zonulin because it is very similar to a protein produced from cholera, which is zonula occludens toxin, which is what cholera does because it opens the tight junctions and, you know, you know, you’re not very well.

Andrew: Locks them open.

Beth: Now, so…pardon?

Andrew: It locks them open. Yes.

Beth: Yeah, yeah. Which is not good. So, the secretion of zonulin is mainly derived from the liver but is also in other tissue, including enterocytes, adipose tissue, brain, heart, lungs, kidney and skin, which I thought was quite interesting. So it has quite a global systemic reaction for us. The physiological role of the zonulin remains to be established completely because it is involved in several functions, including the tight junctions. Still, they also believe it’s responsible for the movement of fluid macromolecules and leukocytes between the bloodstream and the intestinal lumen.

Another possible physiological role for zonulin is protection against microorganism colonization because both normal enteric bacteria and pathogenic bacteria can alter tight junctions. And it has been suggested that the presence of the enteric microorganisms in the small intestine induces a host-dependent mucosal response that leads to the luminal secretion of zonulin. And the enterocytes that do release the zonulin occur in the, I can never say this, the jejunum and the distal ileum but not in the colon.

Beth: Also, whether it hurts…

Andrew: That’s interesting.

Beth: Yes, yes, because I always thought it was the colon and when I re-looked at things, I was like, “Oh, no, it’s actually more the small intestine,” although a smaller bowel. Whether a person has an autoimmune disease or not, it doesn’t really matter because the two most important triggers for zonulin release are bacteria. Some biggies are Clostridium difficile, and Bacteroides fragilis, and gluten. Gluten’s a big one more people would probably know about as zonulin release is stimulated by the contact with gliadin. All right, so obviously, this is very important for those with celiac disease. Still, even people who don’t have celiac disease, the gluten and gliadin proteins found in wheat can still trigger the release of zonulin and increase intestinal permeability.

So this would be something to be mindful of, especially if you know you have a client with non-celiac gluten sensitivity. You know when they’re having gut issues, skin issues, or something else that could show that. Zonulin expression has also been shown to be upregulated in several metabolic inflammatory autoimmune, and neurodegenerative diseases and elevated levels of zonulin have also been identified in children with autism spectrum disorders.

And lastly, good old beta-glucuronidase, I’ve been measuring this for a long time. So this is an enzyme that plays a role in phase 2 liver detoxification, specifically glucuronidation, and also estrogen metabolism and carbohydrate digestion. Now, if we can remember, back to our biochem days, that glucuronidation generally makes toxins and steroid hormones more water-soluble, allowing them to be easily excreted via urine and bile. The beta-glucuronidase is produced by the intestinal epithelium and certain bacteria. So things like E. coli, Bacteroides again, Clostridium perfringens, and the steppe species. And the beta-glucuronidase breaks the tight bond between the glucuronic acid and the toxins in the intestine.

So, therefore, beta-glucuronidase can limit the excretion of the compounds from the body, and that includes medication, as well as hormones, neurotransmitters, and toxins. It actually kind of, like, reverses glucuronidation. It’s too early for me to speak clearly, Andrew, this morning. One moment. Let me moisten my lips, so I can wrap it on them all. Excess amounts of the enzyme can promote or increase the risk of colon cancer too. Because both the incidence of colon cancer and levels of beta-glucuronidase tends to be higher in those consuming Western diets rather than those consuming high fibre, low-fat diets. And that’s been wrapped up in the [inaudible 00:07:09]

Andrew: Okay, so, how many questions? But firstly, when we’re talking about cultures who have high fibre versus low fibre and we’re thinking about the levels of glucuronidase, is this determined genetically, culturally, or is it determined primarily by diet? I’m sorry for a weird question. I’m just wondering about it. You’d probably have to look to transposing the culture too.

Beth: Well, you’re gonna probably have to keep wondering about that. Yeah, because I can’t answer that question. I don’t know the genetics of it or the culture. It’s just really the correlation; I guess because this test is perhaps done more in a western world that people that are eating more poorly or more “Western” diet correlates with…we see more higher beta-glucuronidase.

Andrew: Yeah, yeah.

Beth: There’s probably more toxins that we’ve got to try and get rid of.

Andrew: Well, that’d be true. You also said something very interesting about zonulin, that it has a functional aspect to it as well. It’s not just a dysfunctional or a pathological marker but also a marker of the functionality of our bowel. So I’m wondering, therefore, if we have functional gastrointestinal issues, like, for instance, irritable bowel syndrome. Is there any function of zonulin in IBS, or is it only when we’re looking at inflammatory things? Or do you team it up with calprotectin there?

Beth: No, I would look at all of them. Because even though they all…there’s obviously an inflammation process going on when this happens, but because some of these will, well, all of them can be activated by bacteria. So I can find these elevated in those that don’t have an inflammatory bowel disease or celiac, or they don’t have a known condition that we know is an inflammation. They could just have dysbiosis, and these markers can be out or can be elevated.

Andrew: Okay. Yeah, yeah. So about teaming these three markers together, beta-glucuronidase, calprotectin, zonulin, when would you use these markers as a triad to look at gut function?

Beth: Well, to be honest, I will look at them as individuals on a retest, yeah. But generally, I like to look at those three and other markers in a complete GIT microbiome assessment because of the correlation of enteric and pathogenic bacteria that can affect these things. And what we need to remember is that you know, if we look at them individually, that calprotectin is not specific or diagnostic for inflammatory bowel disease, this is what, you know, I need practitioners to remember, it is not diagnostic, it can be used to detect and evaluate the degree of inflammation.

So you might order these if they have a known IBD and it’s having symptoms. So this may show that there’s a flare-up, and it can detect the disease activity and help evaluate its severity. So then you may choose to treat that or pass them on to their specialists because you would hope that when you get somebody, you don’t discover they’ve got an IBD, that they may have already not had known that diagnosis and are probably on treatment by a GP or a specialist. So then you can help them with the calprotectin is an easy…that can be done as a singular thing to just see how your treatment is going.

Especially if you do a GI microbiome assessment and you see that there is some dysbiosis, so you treat that because generally, the specialist is just going to deal with them with, you know, heavy-duty, anti-inflames whereas we can help them with the bacteria, that is also potentiating that flare up, you know. And also, if a client has had persistent bowel issues with diarrhea with or without blood or mucus, you might order the calprotectin test along with other stool tests to see whether you can rule out whether they need to be moved on to a GP for a potential endoscopy to see if there’s an issue if they have no known disease. Yeah?

Andrew: Gotcha, gotcha. So I would imagine that, from a standard point of view, you know, you’d have your normal path results, your full blood count, your ESR, your CRP, that sort of thing. And then you’d team this sort of thing up to give an indication of trend of benefit of treatment or worsening of their conditions.

Beth: Yes.

Andrew: But I was also very interested because beta-glucuronidase is one of the liver enzymes. Do you team this up with a functional liver detox panel at all?

Beth: No, no, I don’t. I think that’s an excess test. Because if you’ve already getting an elevated beta-glucuronidase, you already know there is some issue with glucuronidation. And so, when I’m treating that, you treat it with upregulating liver function. Because that’s…

Andrew: Okay, so you treat it generally as well. Yeah. Okay.

Beth: Yeah.

Andrew: So I’m just wondering about this protection [crosstalk 00:13:46]

Beth: Yeah, because you got to remember that… Yeah, so I wouldn’t necessarily one begets the other, begets the other; you can look at them as standalone as well as together because I don’t often say that they’ve got the three things going.

Andrew: Okay, because I was going to ask about that, about if there is a procession of these, if you find one rising before the others, like, for instance, upper gastrointestinal issues first and then lower down. But I take your point about calprotectin is in the jejunum and not the colon. So, yeah, let’s talk a little bit further about this. So, do you find that you use them singularly?

Beth: I can do. I can do. And definitely someone with inflammatory bowel disease, I have used calprotectin. Once I’ve done a complete GI microbiome assessment with those markers, then I may use calprotectin as a single to just monitor how my treatment is going. And with, obviously, their feedback. Beta-glucuronidase, as I mentioned, I usually just work with the liver and diet. Zonulin again will be with diet and some gut treatment. But interestingly, with calprotectin, with Crohn’s colitis and small bowel Crohn’s, it’s interesting to note that the calprotectin is somewhat lower in the small bowel. So meaning their level may not be as elevated. And this would be because, as you just mentioned, the small bowel bacterial load, which is the main chemoattractant for the calprotectin release, is far less in the colon, right? And then so less intense inflammatory response you may see.

So you also need to take into account what condition the client has so you can read those numbers. So you’re not thinking that you’ve done this fabulous job because you reduced, but it’s because of the condition is more small bowel. Yeah. And the other thing to be mindful of calprotectin is that it can be increased with intestinal tissue damage and bleeding, which can be seen with overuse of non-steroidal anti-inflammatory drugs, such as your ibuprofen and things like that. So this is where a history and information from a client is very important, not just because they’ve got an IBD that you go, “All right, fine, well, that’s what the calprotectin is about.” If they’re chewing down their ibuprofen, this could be an indication as well. And a low calprotectin will generally mean that it’s not an inflammatory bowel disorder, right? So it might be a viral infection in the gut or IBS. This is usually the IBS versus IBD.

If your calprotectin is not elevated, you’re thinking IBS; if it is elevated, and you don’t know that they’ve got an inflammatory bowel, you would potentially think there’s an inflammatory bowel. But this is where the bacteria assessment is helpful because it could be a dysbiosis that you can treat, and that calprotectin can come down. I have seen it numerous times that we haven’t had to go screaming for an endoscope because I’ve been able to treat them and treat them within four weeks, retest in four weeks, and that calprotectin has come down. If it had stayed up, I would have moved them for some sort of endoscope.

Andrew: Gotcha. Can I ask about fecal testing, microbial testing? I’ve always had this issue that that’s what we see that comes out, not necessarily what’s left in, nor does it tell you where that bacteria came from. So if you’re talking about small intestinal bacterial overgrowth, then you can have the overgrowth of bacteria that would be… Forgive me. That normally resides lower down and infiltrates to an area where it shouldn’t be overgrowing. If you just do a stool test, it’s not going to tell you anything really about where that bacteria is growing, hence the breath tests and things like that. So what do you team things up with? Like, what gives you a clue to go, “I should be looking further at this test, or that test, or this condition?” Like you said like, low calprotectin gives you an indication that it’s not inflammatory? Where do you sort of go, “Oh, maybe I should be looking at SIBO,” for instance?

Beth: Well, that would be with the case history. That would be with the case history. So depending on what they, yeah, but what they present with is…so if I felt very strongly that it was SIBO symptoms, I would go with a SIBO breath test before I would do any of these other ones. I would do that first, treat that to see how we go. I usually will do these markers with a GI microbiome assessment. If the symptoms aren’t really screaming SIBO to me, they’re very lower abdominal, you know, they’ve tried this, they’ve tried that, you know, it’s definitely case history.

This is why it’s very important to really kind of nut out the where. I actually get people to physically show me on their person when they say my stomach or my gut where? Is that a bump to the chest? Is it lower down? That kind of gives me inklings as well. And because other diseases that they may have, right? Because as we know, for example, zonulin, several autoimmune and inflammatory conditions have been associated with elevated levels of zonulin that can increase intestinal permeability. That’s got nothing to do with gluten, you know? I mean, obviously, those with celiac disease it is, but there’s also type 1 diabetes has been associated with high zonulin, has MS, rheumatoid arthritis, asthma, of all things.

So that’s why history is very important. Because the other thing with zonulin too, that you need to be aware of, it is secreted by many tissue. Okay? So you have fecal zonulin, and serum zonulin. And the serum zonulin levels represent a combination of zonulin from intestine, and the other organs, which includes adipose tissue, liver, brain, heart, lungs, and kidneys. And this may explain if you get a serum zonulin and a fecal zonulin result, sometimes they don’t correlate, yeah? Because the serum is more a marker of metabolic disorder such as a low-grade inflammation, or autoimmune, metabolic, whereas fecal zonulin is the better way to evaluate increased intestinal permeability.

And, again, this is another thing, do you do, as you mentioned before, do you go and do this test? So then do I go and do a lactose mannitol test with this? No, I don’t. Again, I think that’s an excess test. I think these tests are privately funded, so the client has to pay for them. And you need to be mindful of what’s gonna give you the best information. And I think if you have an elevated zonulin, and we know that that shows leaky gut, or that the tight junctions are getting a little bit more like fishnet stockings instead of tights, that we don’t necessarily need to then do another test to prove that we have intestinal permeability. You’ve gotta be a bit suspicious if someone’s complaining about, “Oh, my finger, oh, my thumb,” you know, that there’s some inflammation that we need to work with.

And another little thing to be mindful of zonulin is it can be high fecal zonulin in smokers. Okay? There’s a study that showed that cigarette smokers also had higher fecal zonulin, which is, you know, interestingly, because then, obviously, we need to be, again, case history, does the client smoke? This could be causing some of their intestinal permeability. And so a diet’s not gonna help that.

Andrew: No. So this is one of the confounders that you’ve got to take into account when doing a test. But can you tell me if they looked at serum zonulin in the smokers as well and they weren’t elevated? Did they look at that, or did they purely look at stool?

Beth: Yeah, there was something about the serum, again, because it was showing more metabolic stuff. So it was more prevalent in those with higher waist circumference, you know, obesity, blah, blah, blah. But it was more the fecal zonulin for the smokers.

Andrew: Yeah. But that in itself speaks volumes, doesn’t it, about we think that smoking purely affects the lungs. And thereby, you would think that it would increase serum zonulin because it’s a different organ than the gut. But indeed, smoking is directly affecting the gut. And we know that estrogen affects the gut. And I’m thinking here about this quagmire of, let’s say, something like colon cancer. You know, we think of things that are only to do with the gut, like food, but it’s not excess estrogen. It can be involved with colon cancer and things like that. So I don’t know; it’s really piquing my interest with where this might have usefulness. Can I ask…?

Beth: Yes. And I wanted to mention because you just mentioned about estrogen, we need to talk about beta-glucuronidase and estrogen. Because it will typically use, we can look at beta-glucuronidase as an assessment of enterohepatic recirculation of estrogen and inflammation. Because higher levels of beta-glucuronidase have been associated with higher circulating estrogens and lower excretion of estrogens in premenopausal women. And in observational studies have shown a correlation with elevated beta-glucuronidase in certain cancers.

So this is a big thing with estrogen dominance that we can see with people, and that’s what I’m very conscious of my ladies who have some menstrual abnormalities or situations going on. They’re not really abnormal. They’re not quite right, I should say. And I see elevated beta-glucuronidase, I’m straight on to, liver work with that because that can potentially create some of their hormonal issues with the, you know, regardless of their gut, their hormonal issues, due to their elevated…with the high beta-glucuronidase shows us that they’re not necessarily, you know, they’re recirculating, rather than getting rid of excess estrogen.

And it can also be increased with certain medications. The study identified 100 medications that could be reactivated by beta-glucuronidase. And this includes opioids, estrogens, of course, non-steroidal inflammatories, benzos, anti-hypertensive, and anti-diabetic medication. So, again, this is where history is important. Because if someone’s on some of those medications, and they have an elevated beta-glucuronidase, they got double-dosing potentially of those medications, you know, because they’re not utilizing [crosstalk 00:26:49]

Andrew: Yes

Beth: Yes, so again, this is something to be mindful of. Also, a high beta-glucuronidase, as I mentioned before, is being shown in high fat, high protein, and low fibre, compared to more vegetarian or higher soluble fibre diets. Yeah. So it can also be associated with intestinal microbes. So some bacterial producers of beta-glucuronidase will be bifidobacteria, lactobacillus, E.coli, clostridia, Bacteroides, staph. So this, again, is why I like to look at a complete GI microbiome picture. So I’m seeing, you know, and I find out are they a

smoker? Are they on medication? You know, how’s the…if it’s a lady, what’s going on with their menses. So it’s a far bigger picture, and then I’m not just attacking bugs or just going, “Here’s calcium D-glucarate for your beta-glucuronidase and let’s go home.” You know, it’s the whole picture you need to look at.

Andrew: Yeah. The treatment, if you like, that’s coming up time and time again in my mind, of course, is fibre. But I do also acknowledge that you know, you mentioned bifidobacteria there, which is touted to be one of the major, if you like, anti-cancer, probiotics or good bacteria of the gut. But then you get down to the species or even the strain level; it’d be interesting to know which species elevate or decrease beta-glucuronidase or what effect they have. So, let’s go more into treatments now because you mentioned some of them. And one of the hallmarks, of course, is fibre. But what treatments do you find the most effective? And can you strategize them or give them a level one, two, or three for us?

Beth: Oh, okay. Well, generally, if it’s an elevated calprotectin, I’m going to look at…now, obviously, with calprotectin, too, you need to be mindful that it may not be affected by dietary, you know, lifestyle changes, yeah?

Andrew: Right.

Beth: And obviously, if it’s elevated due to inflammatory bowel, then that will rise and fall with that disease activity. If it’s caused by overuse of non-steroid anti-inflammatories, obviously, that will reduce if they discontinue the medication. If it’s due to an infection, obviously, that should come down if you treat the infection, yeah? So, again, you need to know what could be causing that elevated calprotectin so you can be more specific in how you’re doing it. Because using glutamine, which would be my number one, is not going to help if it’s…well, it will help if it’s inflamed, but ultimately you’d have to get them off the medication if that’s, you know, or get them off this, or get them off that, rather than just giving them the glutamine. But I do love glutamine, I love slippery elm, and really, you know, marshmallow, aloe vera, any of those things that are good supplements for gut support and, like we said, the fibre. So various fibres. There’s, you know, the apple pectins, the psylliums, what else have we got in that…? Inulin.

Andrew: Psyllium, guar, banana.

Beth: Yeah. Inulin.

Andrew: There are so many fibres. And of course, our normal dietary fibre which we should be concentrating on as well, so…

Beth: Exactly. Good old fruit and veggie. And some probiotics can be helpful. Good old Saccharomyces boulardii, even Lacto rhamnosus GG, has been shown to be helpful with calprotectin, so that is a species of sorts. Euro lithium is a major microbial metabolite from; how do you pronounce it, ellagic acid?

Andrew: Ellagic acid. Yeah.

Beth: Yeah, which is in pomegranate and berries and that has been certainly showed to help tight junctions as well. So depending, obviously, if there’s some bacterial overgrowth, good old pomegranate comes in handy. Obviously, if there’s a lot of diarrhea, you’ve gotta look at nutrients, you’ve gotta look at their iron, their B12, vitamin D helps with inflammation. You need to look at folate, zinc. You need to look at the nutrients that they could be losing through excess diarrhea, pooing. With zonulin, of course, again with diet, the first thing I would do is take them off gluten regardless. You know, I say, “Let’s try that.” But also, if they’re doing a lot of simple sugars, basic sugars that can irritate lots of salt. Emulsifiers can also be triggers for zonulin release. So you would definitely look at diet there. Also, I’d look at things that are anti-inflammatory, so that’s things like quercetin, vitamin C, vitamin D, curcumin, beautiful curcumin, gamma-linoleic acid, your omega-3s, aloe vera I mentioned before. God, my lips aren’t working today, are they?

Andrew: De-glycerized licorice.

Beth: That’s it. Let’s call it DGL.

Andrew: DGL. Let’s just say…

Beth: Even collagen is helpful, too.

Andrew: Okay.

Beth: Yeah, and of course, zinc is good, but glutamine is probably gonna be my go-to with mainly the calprotectin and zonulin. Beta-glucuronidase is the generally the fibre and something that has calcium D-glucarate in it. Which some, you can get that as a single entity or it is in various gut supplements, but sometimes it won’t be listed, do you know, because it may be as an excipient, not as a, you know.

Andrew: Yeah, because what was its secondary name? Its calcium saccharate was its equivalent name.

Beth: Okay. I did not know that.

Andrew: Yeah. So some companies use to get around TGA legislation by adding it as an excipient named calcium saccharate.

Beth: Excipient. Yeah.

Andrew: Yeah, yeah. It’s always been a good

Beth: Yes, and so it would pay to ask your suppliers, you know, rather than just giving…

Andrew: But in this respect, dose is really critical, though. You’ve got to use an appreciable dose to get an appreciable effect.

Beth: Oh, absolutely. Absolutely. And that’s why you would also look at the diet. So that’s the other thing. If I have someone who has high beta-glucuronidase levels, I will also really go through their diet, put them on a “detox,” you know, a lighter diet to reduce the fat, reduce processed food, reduce sugar, reduce alcohol, reduce smoking, that sort of thing. To help, because, ultimately, I don’t want them on supplements forever. So if they can do what they can with their food is helpful. And then we just turn down the inflammation a little bit without glutamine, and what have you.

And obviously with beta-glucuronidase because it is liver, you know, you’d also perhaps look at herbs like St. Mary’s thistle, bupleurum, Schisandra, dandelion, nutrients such as your choline, inositol, methionine, glycine, cysteine, things like that. And I will usually do this in a supplement that has all of those things in it rather than individual because, again, I try and make it more practical for my clients, so they’re not having 1001 tablets or potions or powders. Because sometimes they may be doing this for, you know, weeks, depending on their level of elevation of numbers.

And so that’s where these individual markers can come in, is rather than having to do a whole GI microbiome assessment every time, you can just… So that’s what I will do is I will just check the calprotectin or the zonulin levels to see that they’ve come down, so I know we’re on the right track. Yeah. The other fibre that I like is glucomannan which is from konjac.

Andrew: Oh, well done. Konjac, glucomannan.

Beth: Yeah, konjac is quite interesting, because apart from supplements that you can get it in, they make low-calorie noodles out of it. So all of those people are…

Andrew: Oh?

Beth: Yeah, so you can get skinny pasta or whatever it’s called, thin noodle, skinny pasta, and it’s made out of konjac. So that’s [crosstalk 00:36:35]

Andrew: What about the taste? What about the texture?

Beth: No, yeah, it tastes like wet konjac. But if you put tasty additions to your noodles, you know. But that’s another way of getting it in the diet is actually using the konjac noodles. So, yeah, and you can always sprinkle other things on there.

Andrew: Can I just go back to something that you were speaking about right at the beginning with zonulin that it’s seen in non-celiac sensitivities. This was something that Alessio Fasano, I spoke to him about. So, like, talk about a bromance with that man. I was so enamored by him. But it was really interesting how Alessio Fasano and David Perlmutter, David Perlmutter was of the mind of, “No gluten ever just get off it, say goodbye to it. It’s bad for everybody.” Alessio Fasano, I questioned him about it, and we were talking about that you’ve got celiacs, then you’ve got this extra population that has non-celiac gluten or gliadin sensitivity. And then you’ve got the people that can handle wheat. And there’s no issue whatsoever.

And so I asked him, I said, “Do you think it’s appropriate if you like, that we just take people off wheat if we see increased zonulin? And he said, “No, look further.” So it was just an interesting thing about his way of dealing with, I mean, mainly kids with his practice in hospital over in the US. But I’ve just thought it was a really interesting point that he’s of the mind; no, no, he’s not paranoid about all wheat, but he does accept that there’s a greater proportion than celiacs that have a gluten sensitivity.

Beth: Yes, yes. So, yes, I mean, I’m a bit that way too. I’m not gluten is the devil because it’s not. Because myself and other clients that I’ve had could eat bread, pasta, pizza, croissants in Europe. I ate, you know, it was carb heaven, and I didn’t have any issues with my gut. Whereas if I did that here, I would be going to see myself because of my gut issues. So I sometimes think it is the processing of the wheat, not necessarily the wheat itself.

So this is why I think demonizing a…I don’t like demonizing a particular food at all, except gluten. If you’re a true celiac, then absolutely. But otherwise, it’s the same as peanuts. If you’re a true peanut allergy, then they are demons. But otherwise, I think demonizing food; there’s already enough trouble with people with food issues. What’s it called? Not anorexia, whatever it’s called. Where they

Andrew: Anorexia nervosa, bulimia.

Beth: Yeah, but now the one where, orthorexia, where it’s just, they limit their diet so, so much. They’re either paleo or keto can only have this; the vegans only have these. They’re larger groups. But then you have the people that have

got, “This upsets me, that upsets me, I’m “allergic,” to all these foods.” And, A, is the wrong word to use.

Andrew: Gotta love that term.

Beth: Yeah. And then people just limit their intake. And so then they’re more likely to get some of these issues because of their diet. Do you know what I mean? Because their diet is restricted, then that can affect the bacteria and what have you, loads, which can affect them the release of some of these nutrients.

Andrew: Yep. You make a very good point about the cultural aspect. For instance, bread is made in Australia and/or America, versus how bread is made in the European countries, or indeed, you know, let’s say South America, let’s say, Africa. How because it’s a non-commercialized, non…what do we call it, mass-manufactured product, it’s a more personalized, much more bacteria, fungal, yeast-led fermentation, rather than this pure, fluffy white cloud. It’s a very interesting point.

Beth: Yeah.

Andrew: Yeah, but it’s very interesting point. You said that over in Europe, you just didn’t have this issue.

Beth: Oh, no, I had a field day over there. It was wonderful. And there’s even a pizza restaurant that I go to here in Australia. And I said to her, I said, “Oh, I love your pizzas because blah, blah, blah.” And she said, “Yes because they get their flour from Italy.” They don’t use Australian flour. They literally import it from Italy. So then that, to me, means that it is various processing, you know, potentially processing things rather than the actual food. So, yeah, I don’t like to demonize food, and I will reduce gluten. Generally, what I will say to clients is that when you are in control of what goes in your mouth, maybe you avoid that. But if someone invites you out for, obviously, if you live anywhere else, but Melbourne and someone invites you over for dinner, you can go. And if they deal you up with pasta, you eat it. Do you know what I mean?

Andrew: Yeah.

Beth: You know, because I usually say to people, “It’s one meal out of 21 a week.” So you should do that.

Andrew: Well, so there is an interesting point about, we’re talking about beta-glucuronidase, we’re talking about liver work. And you know, one of the interesting bile acids that has far-ranging consequences, deoxycholic acid, so do you incorporate digestive enzymes? You were mentioning herbs that stimulate bile acid flow, but also things like lecithin, for instance. Do you incorporate these at all?

Beth: I’ll definitely use digestive enzymes. And, again, with some of these GI microbiome assessments, they will actually look at pancreatic elastase, which is a digestive enzyme marker. So if that’s a little bit subpar, I will definitely introduce the enzymes. So it’s case-specific. Sometimes yes, sometimes no, depending on what else is going on. Yeah.

Andrew: Sure. Beth, where can we find out more information about this? Obviously, there’s a lot that goes on with case history. So you’ve always gotta rely on the case history as the backbone to any concept.

Beth: Very much.

Andrew: But where can we find more information about beta-glucuronidase, calprotectin, and zonulin.

Beth: You mean apart from Dr Google?

Andrew: Apart from Dr Google, please?

Beth: Yes. All jokes aside, there is actually plenty of information on the net. And a lot of great studies on PubMed. Yeah, so go into Google Scholar and just go for it. There’s heaps of studies on this stuff, heaps of stuff on zonulin, calprotectin, and beta-glucuronidase. Also, there are several labs that do these markers in tests and do GI microbiome testing. So, obviously, they would have lots of information to look at as well. So, yeah, that’s generally the kind of go-to places that I would look at.

Andrew: So we might choose some of these more important ones and put them up on the designs for health website in the show notes for people to look at and learn from. Beth, thank you so much for taking us through this today. It’s obviously, you know, it’s bigger than “Ben-Hur” when you’re looking at trying to get three tests and tell you the answer, the truth. Can I just ask one quick last question, and that is you mentioned a glib comment about how patients say they’re “allergic” to foods. Obviously, there are those people who are truly allergic to things like peanuts, fish; we know the usual, eggs, the usual culprits. But how much time do you have to spend educating people that they’re not allergic, necessarily, to a certain food and that they’re sensitive to food? How do you get around that term allergic and start to educate them about food sensitivities rather than allergies?

Beth: Well, it’s pretty much exactly what I say. I say true allergy is something like bee sting allergy, or the peanuts, or the gluten. And that otherwise, we have sensitivities. You know, that we may be, because of too much of something, like if you eat too much of something, obviously, then the body goes, “No, thank you very much.” Or, and sometimes too, I have to educate people that it may not necessarily be the food, right? Because as I said, people demonize food, like, you know, they had chocolate, and, “Oh, my God, chocolate did this.” Well, was it the chocolate? Or was it that you had three serves of wheat that day, and then you had something else, and then the chocolate was what tipped you over? You know?

So there’s, like, a cumulative effect rather than the other. Or sometimes, if people go, “Oh, it’s this,” and I say, “Is it always x?” And people go, “Oh, not always.” And that’s when I’ll dive in and say, “Well, then that’s when it’s not necessarily the food, but it’s your gut, because your gut’s reacting to a multitude of information that it’s had coming into it,” you know.

So people are usually more open to hearing then go, “Oh, okay.” And then I say, “So let’s look at your gut,” rather than, you know because back in the day, it used to be that people just wanted to do an “allergy test.” And it was like, well, I found that when people did that, I go, “Yeah, okay, you can spend your bucks and do that, but I can pretty much say that you’re gonna react to most of those foods.” Which they do because their gut is inflamed.

So or sometimes I might say to someone, it’s like if you’ve got a scratch, like, a bad scratch if you keep scratching it, it’s not gonna get better. And if you put things on it, you know, it might be salt stings or something else. But it’s the scratch that needs fixing. It’s not what you’re putting on it. It’s the scratch that needs to heal. Do you know what I mean?

Andrew: Yeah.

Beth: So yeah, so generally, I find that if I explain that, it doesn’t take very long for me to explain that; it’s more about, “And this is why we wanna look at your gut,” rather than tell you you can’t eat this, you can’t eat that. There’s too many people that are already on restrictive diets, like the FODMAPs. That’s a-whole-nother conversation. FODMAP diet, and they find out they’ve been on it for 12 months. I find it very hard to then reintroduce foods to those people because their gut and their gut microflora has got used to a particular diet.

Andrew: But that’s a whole other podcast about antigenic, forgive me. Let me say that one again. That’s a whole other podcast about antigenic ambivalence, isn’t it?

Beth: Yeah.

Andrew: And teaching our gut to not react to certain foods. Beth, thank you so much for taking us through this today. There’s obviously so much more that we could cover. But, yeah, thanks so much for taking us through the sort of salient points to do with beta-glucuronidase, calprotectin, and zonulin in gut health today.

Beth: Absolutely. My pleasure.

Andrew: And thank you for joining us today. Of course, you can find all the show notes and the other podcasts on the Designs for Health website. And we will put up certain relevant papers, of course, so that you can learn from them today. But thanks so much for joining us today. This is “Wellness by Designs.” I’m Andrew Whitfield-Cook.