Wellness by Designs - Practitioner Podcast
Wellness by Designs is a place for healthcare practitioners to expand their knowledge base. A place to deepen your nutrition, herbal medicine, naturopathic, integrative medicine and business management expertise. Sit back, grab a cuppa. Wellness by Designs has your continuing education covered. Tune in as fellow practitioners, and researchers share their expertise and clinical pearls, taking you on their professional, sometimes personal journies. For show notes and references: www.designsforhealth.com.au
Wellness by Designs - Practitioner Podcast
ENCORE: Unlocking the Health Secrets of Vitamin K2 with Dr. Brad McEwen
Discover the exceptional benefits of vitamin K2, especially its form MK-7, as Dr. Brad McEwen, a naturopath and nutritionist, joins us to reveal the nutrient's essential roles in our health and wellness.
Gain insight into the unique structural and functional differences between vitamin K1 and K2 and how these contribute to our bodily functions, from bone health to cardiovascular wellness. Delve into the potential positive impact of vitamin K2 on chronic conditions.
This episode unpacks the incredible ways vitamin K2 serves as a director of calcium in our bodies, guiding it to strengthen our bones and keep our arteries clear of calcification. We'll explore the critical synergy between vitamin K2 and vitamin D3 for chronic disease prevention and the science behind the activation of bone mineralization proteins.
Dr. McEwen shares valuable knowledge on the importance of monitoring vitamin K2 levels for optimal health and why it's imperative for practitioners to stay well-informed through ongoing research.
About Dr Brad:
Dr Brad McEwen, PhD, is a leader in preventive and personalised health, particularly in the area of cardiometabolic health and mental and cognitive health. He is an award-winning naturopath, nutritionist, herbalist, educator, researcher, and mentor with over 24 years of clinical experience. He has a PhD from the University of Sydney, a Master of Health Science (Human Nutrition) and a Master of Public Health from Deakin University, among other qualifications in nutrition and sports medicine. He has a passion for teaching and has been educating in nutritional and naturopathic medicine and the health sciences for over 20 years. He has extensive experience in presenting seminars, webinars, and at conferences nationwide and internationally,
Brad has a passion for research. He has published numerous original research and review articles in peer-reviewed journals. He is a peer reviewer for international journals. His research interests include the effects of diet, nutrition, and lifestyle medicine on cardiovascular disease, cardiometabolic syndrome, depression, anxiety, polycystic ovary syndrome, endometriosis, cognition, stress, type 2 diabetes, and chronic disease.
Connect with Dr Brad:
Website: https://www.cmgrouponline.com.au/
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DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health
Music. This is Wellness by Designs, and I'm your host, andrew Whitfield-Cook. This is Wellness by Designs and I'm your host, andrew Whitfield-Cook. Joining us today is Dr Brad McEwan, a PhD naturopath and nutritionist who works with the Complementary Medicines Group, and today we'll be discussing all about vitamin K, mk7. Welcome to Wellness by Designs, brad. How are you?
Speaker 2:I'm very well. Thank you very much for the introduction. How are you?
Speaker 1:I'm great mate. Very good Now. First of all, we need to differentiate between the vitamin Ks, because it's one of those much misunderstood molecules, particularly in medical circles, who still don't realise that there's more than just vitamin K. So can you take us through the different side chains, the different molecules? What is vitamin K and what is vitamin K2?
Speaker 2:So, first off, I'd like to start by saying I'm very excited about doing this podcast and I believe that you know everyone should have have some. Everyone should have some vitamin k2. And, to finish off with that, thank you very much for all your attention. Sorry, just a side joke. So the exciting thing about exciting thing about vitamin k2, as what you're saying, andrew, is, it's a very wide field of information and if you think of it in a way as, yes, there's vitamin K1, vitamin K2, but why should everyone be having some and what is so special about it? And one of the areas I want you to think about is let's start back at the beginning looking at structure, function, biochemistry. Put that in your mind as we go through today's journey I'm going to say today's a journey through vitamin K2, because we're going to cover a wide range of different areas. So, as we go through, think of structure, function, biochemistry and what's linking all these things together, because if you understand that, you'll have a better understanding of, you know, health and nutrition and sort of naturopathic medicine in general. So when we start thinking about, you know, vitamin K, vitamin K2, cetera. What is it? So the two main ones we look at is vitamin K1 and vitamin K2, named normally in numerical order, as, like the B vitamins, it sort of goes in order of when they're found. So one thing I want you to think about is vitamin K1 has a vital side chain, so it's sort of like a lipophilic side structure and that's its main differentiating point, while vitamin K2 has more like a carbon chain, carbon bonding type of effect, where we're looking at sort of these repeat molecules, and that's the main difference structurally between the two. I know it sounds sort of simple One's more of a lipophilic and one is more of a sort of carbon-based structure. But that actually helps benefit the differentiator. Two of how they work.
Speaker 2:And we always see things like you know what is the difference between minoquinone 4, minoquinone 7, minoquinone 10? There's all the way from sort of number 2 to number 14. And that's all based on the number of side chains. So there's your biochemistry. Very easily, it's just a simple thing. As in, how many side chains does this have?
Speaker 2:And in this case, menaquinone 7, which is the focus of what we're talking about today, has 7. So I want you to think sort of you know, how do we get this? Where does it come from? So vitamin K2, particularly metaquinone 7, is formed in the gut. It's formed in our bacteria, so we can actually manufacture part of it ourself and in fermented foods, of course, from the bacteria of the fermented foods. So that sort of takes us back to you know, it all happens in the gut effect. You know how we talk a lot about naturopathic medicine is a lot of symptoms and systems, I should say, work from the gut out, inside out. So if we keep that in mind, that's a very big area. If we have good digestive health, we'll have better digestive health related to our vitamin K2 metabolism, particularly in Medicare 7.
Speaker 2:So I want you to start thinking about comparing the pair if you think about this. So Medicare 7iQ7 is, we're looking at, absorbed in the large intestine, while vitamin K1, phylloquinone is actually absorbed into the small intestine. So it's sort of like the small differences. To start with, and as we go through the different processes, vitamin K1 and vitamin K2 are both sort of absorbed and utilized into our chylomicrons, into our ldl cholesterol as well. So we always tend to think of ldl cholesterol as being, you know, the bad guy causes all these problems. But I try and think, hang on, ldl actually does play a role on the body. It's very useful for, um you knowuble vitamin carrying, such as K2, but also other nutrients as well, throughout the body, so it actually has a wider role.
Speaker 2:So if you think about this, vitamin K2 and K1 gets absorbed in our gut, gets attached and enveloped, I suppose, by the chylomicrons and deposited throughout the body, and particularly with K1, it goes into the body, gets picked up by the VLDLs and gets taken back to the liver where it tends to, let's say, live its life.
Speaker 2:Vitamin K1 particularly does a lot of functions in the liver. The difference with vitamin K2 is it tends to utilize the LDLs a lot more easily and transport to what we call the extra hepatic tissues that are outside the liver. So vitamin K1 stays inside the liver. Essentially, after absorption, vitamin K2 goes throughout the body, and that's what makes it different as part of our clinical side that we'll talk about later. The other thing that's exciting about vitamin K2 is it crosses the blood-brain barrier. So that's something we can start thinking about later on when I talk about plaque forming and crystal forming conditions think of alzheimer's or multiple sclerosis, etc. That it can actually have greater benefit in. So everyone always thinks with k2 is blood and bones, which is good good to think that way, but what we'll be talking about in this podcast is, you know, a little bit more than that yeah, okay.
Speaker 1:So a couple of questions straight off the bat. If we're talking about in uh mk7 being incorporated into the ldl molecule, does it have any protective effects there, like, for instance, ubiquinol does, protecting the LDL particle against oxidation and therefore foam cell production? Do we have any evidence that MK7 has that sort of protection against atherogenic molecules?
Speaker 2:It's an area I haven't looked into yet but it's quite exciting because I like the ability of how vitamin K2 does have that antioxidant effect and cell protective effect. And if you were to combine it with ubiquinol, tocotrienols, for example, and other similar antioxidant molecules, you could predict from small, dense LDLs like the golf ball effect of it smashing into the arterial walls. Like the golf ball effect of it smashing into the arterial walls. So from my thinking of going back to, like I mentioned earlier, our structure function biochemistry, short answer is yes, I think from what we understand, it will do that. It's not an area I've looked into but I will now. But it's something that I think will actually make a big difference of our understanding of how vitamin K2 does that work.
Speaker 1:Yeah, and another one. Sorry, brad, to go straight off the bat, because you piqued my interest, and that was when we're talking about being incorporated or helping the liver. Do we have any evidence yet that vitamin K2 MK7 might be beneficial in conditions, metabolic conditions like, um well, we used to call it non-alcoholic fatty liver disease, but we realized that there was too many people drinking not having none, um, so I think the acronym is now massaled. Is that right m something?
Speaker 2:like that. Yeah, there's a lot of metabolic associated.
Speaker 1:Metabolic associated don't know what the host in their liver disease muscle. Um yeah, I think the acronyms change, but do we have any evidence yet that MK7 is a benefit in those conditions?
Speaker 2:not that I've seen particularly like related to what you're saying, but if you look at the wider aspect of how non-alcoholic fatty liver disease or fatty liver disease, cirrhosis or any of these liver diseases work, the short answer again is yes, I believe it will actually have great benefit in that area because it is working through the regulation of cholesterol metabolism, antioxidant, anti-inflammatory pathways, calcification pathways, which I'm about to talk about. So I do think that we are going to see more benefit in that research. The main sort of focus of research of K2 that we'll be covering has been extrahepatic. They haven't really been looking at the liver. But if you think of the vascular system, of course the liver is very highly contained of vascular tissue, so that's how part of the filtration unit affects. So with my understanding of how it works, it would definitely greatly benefit.
Speaker 2:And there is research with tocotrienols, for example, of reducing the impact of non-alcoholic fatty liver disease or fatty liver disease, adiposity-based conditions, which is where there's a new condition-based ABCD they call it, which is sort of adipose B, because I can't remember, because I just thought of it cardiovascular disease, like they've tried to do like an alphabet kind of thing where each letter means something and it may have an adipose based. It may be as simple as that. Um, yeah, right, but it's where you start thinking about. You know, when we do have adipose tissue, whether it's in the gut or the liver or around the heart or brain or any other area, you know it's on fire and it's causing some inflammatory effects and if you think of any way that can greatly benefit the blood flow. The antioxidant, anti-inflammatory capacity which vitamin K2 is working in the background of, I think it would greatly benefit in those situations.
Speaker 1:Yeah, Okay, so K2, then we've got the different molecule lengths. We don't have it here, as is my understanding in Australia, the MK4. The one that we have available is MK7, but the molecule lengths go right up to what? 13 or something. Is that right?
Speaker 2:So 13 and recently 14. So we're finding, you know, a lot more research as we go through, and that's the benefit of you know where we're going with nutritional medicine and naturopathic medicine in general. So it's not just science. You know research, of course, but it's how we apply it and that's where, in the year that we're in, it's very exciting to see a lot more research come through.
Speaker 2:And there is some MK4 research out there, so metaquinone 4. They tend to call it MK, so metaquinone, k2, and then they break it down into its numbers MK7 is metaquinone 7, metaq7. So if you think about it, the lower the number, the shorter the molecule, the longer the number. You know the long chain kind of effect. So if you keep that in mind, that seems to be the way how it works in the body where the long chain kind of effect. So if you keep that in mind, that seems to be the way how it works in the body, where the longer numbers seem to be more flexible. So particularly mk7, metaquinone 7, being in that mid-range, it is classified as a long chain vitamin k. So I want you to start thinking about long chain fatty acids etc. It's the same kind of thing with k2, is you've got different lengths doing different things and a lot of the research is still based on this sort of menoquinone 7 effect because they're finding that's where it has the greater effect, because it seems to have that sort of more bio flexibility of the molecule compared to the longer chain and the shorter chain and being in the middle it seems to have that greater effect even though, as I said, it's still classified as a, as a long chain.
Speaker 2:And what I'm thinking about is, as we go through this podcast and general conversations is, um, there's always new ideas coming up, like the more we think about with you know, biochemistry, and it's a very good question, you know, with the length of the structure and how it works in the body. Um, again, thinking of tocotrienols with the bifatal structure and how it works in the body. Um, again, thinking of tocotrienols with the biphatal tail, it's able to move its way into the fatty tissue, into the cell membrane, work antioxidant inside and outside, anti-inflammatory inside outside, outside in. So it sort of goes both ways. We're finding that a lot more with vitamin k2 now is it's I'll use the word biphasic, where it's able to sell signal inside out and outside in to incorporate a lot of these changes. It's quite exciting right?
Speaker 1:yeah, absolutely. If we're thinking about food sources, though, like I have not looked into this at all with regards to chain length, all I'm aware of is things like natto hence natto farmer, but from the natto beans with what is a bacillus subtilis fermentation. And then there's cheeses, as well Swiss cheeses. I don't know of any other source and I don't know about if either, or which foods are more linked with different side chains. Do we have any knowledge of that? Like you said, like we've now elucidated, a side chain of 14, so an MK14. Do we know what foods that's from? Or is that only from, like, fermentation of bacteria in the gut?
Speaker 2:Seems to me more from fermentation in the gut, but also they're finding it in some fermented foods. So, going back to the natto, which is a fermented food, I'm thinking, you know, let's jump ahead or back in this case, things such as, you know, sauerkraut and other just general fermented foods that have been around a long period of time. We've always used them for digestive health for centuries and not really knew how they worked, and we're still finding out more and more details about fermented foods. So it makes me think, you know, vitamin K1 is mainly found in green leafies, for example. That's one of the main sources of it, as we were working on earlier, and K2 is more in fermented foods. So I'm going to suggest any major fermented food with that sort of bacillus that we were just talking about. That seems to be where it's found and again in our gut. So we've got a whole ecology working with us or against us in some cases, that could be working with metabolising.
Speaker 1:Yeah, okay, so the uses, if we go into, I think the initial work was done on bones, but then it took a side thing and was looking at cardiovascular disease. There was other potential uses as well, depending on the. What is it the proteins they're working on? Is that right?
Speaker 2:That's right. So there's a number of different areas. So what I was thinking of because when we were originally talking about this, I was thinking how can we go about, you know, discussing the benefits of vitamin K2 in a short amount of time, because we could talk all week about this, and I was thinking let's go through some base health conditions first and then sort of you know, expand on those. So the main functions or uses, of course, is improving bone health. That's one of the main areas that they looked at. You know, reducing fracture risk there's a lot of research on that. Vitamin K2s Everyone always thinks of, you know, calcium and vitamin D. That's great because that does have a lot of evidence in phosphorus or phosphates for the bone structure matrix. But you also need something to sort of direct and work things out, as in I see vitamin K2 as a director in a lot of these areas. So whether it's blood, bone, other tissue we're about to talk about and that's what I like and find exciting about vitamin K2 is that it is like the director. So we've got other areas such as blood coagulation, which is well known. We keep looking back into that. Just overall, cardiovascular health reducing cardiovascular risk and mortality, reducing vascular calcification, which we're going to be talking about shortly, reducing arterial sort of stiffness. So I want you to imagine the cardiovascular system is like a hollow tube, as we know, and if the hollow tube is flexible and flowing properly, we have good blood flow. Once it becomes sort of stiff and sort of more restricted, that's when you get your hypertension's and your hemorrhages and your vascular depletion, strokes, heart attacks, dvt, etc. Um, metabolic syndrome. There's a lot more research there where vitamin k2 is working hand in hand with insulin, which is pretty cool. So, remember, we're moving away from the original side.
Speaker 2:Now, improving chronic kidney disease, which could also be related to, you know, type 2 diabetes, vascular, yeah, wide range of different health conditions. Of course, with chronic kidney disease, kidneys are very tough. You don't normally notice there's a problem until there's a big, big problem and, yeah, they don't feel pain too much. So therefore, they have to be really large or really small and sort of I'll use the word damaged for them to actually tell you that there's a problem with themselves. They're quite tough. And also just reducing age-related chronic disease states. We're finding out. So, you know, in the last decade or so there's been a very big push for vitamin d3 and you know vitamin d3 markers and having x amount of um in the blood, for example, when you do a blood test should we be also measuring for vitamin k2, because they work in a similar pattern of chronic disease prevention or risk reduction?
Speaker 2:So I was thinking, sort of taking us on a bit of a journey through vitamin k2, if you like, about how it works. I like stories when it comes to this because it helps me remember how it works. So I want you to start thinking about. You know, vitamin k2 is a multifunctional molecule, multifunctional nutrient vitamin. So yes, it starts with the bones that's where we know but actually starts working in a lot of wide range areas as well.
Speaker 2:So it works with a lot of enzyme pathways. So one of them's and I've written down some notes, I remember how to say them right gamma glutamyl carboxylase enzyme pathway, which sort of works with glutglutamyl carboxylase enzyme pathway, which sort of works with glutamic acid. So carboxylase is glutamic acid. So COOH bonds, et cetera. It seems to work with functionality there. It works with I love this name vitamin K dependent proteins. I'm like whoever thought of that name one day was on fire. It's like naming Sydney Harbour, sydney Hardney harbour bridge and sydney opera house and sydney cove. Like those people get paid big money um great sandy desert great sandy desert, let's get gum.
Speaker 2:Um. Western australia, northern territory, south australia. You did really well. So. So this day this person was on fire and called them vitamin k dependent proteins. So that really works for me. So it says what it is.
Speaker 2:So one of these particular proteins that works with the I'm going to call it the glutamization new word of the day doesn't exist. Glutamization is osteocalcin. So we do know osteocalcin. So if you, whenever you're trying to understand a word that you've never heard of and this is for a lot of our viewers who may be starting off in their careers break it down Osteocalcin, osteo normally meaning bone calcin, calcium, so transportation of calcium, and it's synthesized by the osteoblasts. The osteoblasts, of course, are bone cells that form and create things. This is forming during mineralization phase of the bone. So osteocalcin is very important for bone health and it binds to the calcium ions and the hydroxyapatite crystals, regulating size and shape. So I want you to imagine because we're going to stick with the bones and start with the bone matrix One of the main stages of working on bone matrix is between the ages of eight and 10.
Speaker 2:So, andrew, you and I are a little bit gone past that point of ages eight and 10, but we can still keep working on the regulation of that because up until about the age of 21 to 25, which is the category that you and I are in it seems to be still forming and working to get that sort of solidification for the rest of our life. But what I want you to remember is we're always building, breaking down. Nothing is ever set in stone, so to say, because red blood cell is 120 days, like platelets 7 to 14 days, like things are always growing and developing. We're growing and developing from the moment we're conceived, the conception of who we are, all the way to the end. We're always growing and developing in all different areas. Everyone always seems mentally and physically, for example, and emotionally growing. But physically the body and the biochemistry is always growing and developing. So our bone is always in this constant state of flux, where it's always moving and it's regulating and it's changing. So if you sit down and do nothing all day, your bone mineral density will change, probably go to your buttocks, because you're sitting on it all day doing nothing.
Speaker 2:But if you get up and become active and that's the comment I made about ages of 8 to 10, up to 11, because you're physically active and you're actually impacting and pounding on that bone, and gymnastics and tennis and a lot of these force activities create that bone strength. Swimming doesn't, of course, because it's not weight-bearing those kind of activities, but anything that's moving, including just walking, starts that process. Swimming doesn't, of course, because it's not weight bearing those kind of activities, but anything that's moving, including just walking, starts that process. So getting up and moving, and that's when we start to develop and those crystals then start to form and our bone starts to form shape to where it needs to be. So, whether it's a long bone or a finger bone or anything else like that, again, it's the old if you don't use it, you lose it kind of mantra that we say with a lot of things. So if we keep working with this osteocalcin and this is where we start to visualize in our mind that it's sort of creating a higher affinity to this hydroxyapatite mineral bone content and it's actually driving in calcium and other nutrients, of course, into the bone tissue and that's what we really want. So I want you to start thinking. This is like a link between geochemistry and biochemistry now. So I want you to start thinking, because you know geochemistry is all crystal formation, minerals, et cetera. So in some cases some people are just big walking crystals. You know, I want you to think about that. So they've got the bone mineral density that's changing. They may have gout, which is crystals as well. So there's a lot of areas that sort of start thinking about crystal formation and it's going to the wrong place.
Speaker 2:And osteocalcin, being driven by vitamin K2 and of course vitamin D3, is working on this journey. So again, we're sort of working with visualisation of bone forming and other tissue utilising it and if we think of that process we can start thinking about what else happens. So osteocalcin then starts working with energy metabolism, bone metabolism, endocrine function. So all the different endocrine organs are starting to become involved. So this is all part of our metabolic health, because our bones are metabolic, our blood is metabolic. So if you think about regulating energy metabolism and just overall health, that way it starts working.
Speaker 2:And another role which we'll talk about later is it has this inhibitory role on angiogenesis. So angiogenesis, of course, is the formation of new blood vessels and we want that to happen for general health, but we don't want that to happen in cancer, because the generation of new blood vessels means blood flow for the cancer cells, which means growth and development of them, leading to cancer formation. As a brief storyline, it also regulates ectopic tissue calcification. So ectopic always means away from sort of where it should be. So in this case we're talking about blood vessels. So there's a wide range of different areas that we're working of, just with the osteocalcin side, and it's a transporter, and we're journe, just with the osteocalcin side and it's a transporter, and we're journeying through the body, and that's what I like. Start to thinking about all these vitamins and minerals and amino acids and everything going on a journey for our for our nutritional needs. Yeah, there's another protein. There's the matrix GLA protein that keeps working with this and that works with the cardiovascular disease health um.
Speaker 1:So the matrix GLA proteins. Brad, can you tell us more about those, what they do so?
Speaker 2:again I want you to think about. You know the terminology matrix, GLA. So we always talk about the matrix, not the movie, but the actual matrix in the body, where it actually works by. It's like a netting, a structure. It's hard to explain sometimes without using too many hand motions Cellular matrix, tissue matrix, organ matrix.
Speaker 2:It seems to work by, you know, piecing and putting things together into its cell structure, into its system, and that's what I find interesting, where there's this communication between cells that are the same cell but also other cells. The body has this amazing communication with itself. It's just and again, in today's year we're still finding out the way, how. You know, I'm fascinated by how things work, how we can talk and think and walk and text and do all the things all at the same time. And it's the body's, you know matrix system itself working and communicating with each other. And this gla matrix is one of those areas and what I was thinking about, as I mentioned earlier, sort of going through a bit of a journey into um. You know, applications of, of how we could utilise, you know, menaquinone 7, K2, and you've got to say it's low.
Speaker 1:So the evidence we started off with earlier work by Thuisson and his group. What is the evidence now showing us? Because there was some positive, some negative evidence, but when I looked further it was kind of like what was one of them there was a positive change in the lumbar vertebrae but a negative change in the. Was it radius, radial density, radial bone density? So it's almost like what you were talking about earlier about that need for exercise. Now I don't know about this. It was just an interesting thing. Tell us more about the research and where it's leading us.
Speaker 2:And that's the exciting thing. There's a lot of interesting things that we can really move into as we go through and I want you to think back. Most people now are becoming more sedentary over the last few decades. We're working more inside, less active. I have my Apple Watch, where I deliberately have it set, where I have to get up regularly and move around so that keeps circulation going, keep the body going metabolic-wise, and that's what I'm thinking back to, that study that you're mentioning, that the lumbar region is being used more because you're sitting on it, for example, and you're using it more as weight-bearing.
Speaker 2:While your wrists may be on the desk, they're not really working as much. You may be typing or using the mouse, but it's not weight bearing as compared to your lumbar. But if you start exercising more and actually moving moving and grooving and moving around, you start to use that. That's where some people use weights, you know, like the wrist weights or just do that. That's weight bearing still, um yep, so holding it using a mouse is not weight bearing, but it's sort of like any kind of activity. So you know, if you need to get up from your desk and do like the old 1980s sort of aerobic exercise around the office where you're punching the air and moving around, because that sort of gets things up and moving and then you can add some weight bearing to that. Um, so what I'm thinking if I go through some of the research that this is leading to, and then we can have a good discussion at the end, because it's sort of quite exciting where, where we're going, and part of that is, of course, you know, cardiovascular disease. We're looking a lot more vitamin k2 and quinone 7, cardiovascular disease. So one of the areas I mentioned earlier is coronary artery calcification. So what is it? The name it says we're very well named. Coronary artery is calcified. There's a calcification process happening and it's a very significant predictor of cardiovascular disease and cardiovascular disease risk. And there's some pioneering work in that area where you can look at calcium scores et cetera. So one of the areas we've been looking at is a deficiency of vitamin K2 has been linked to vascular calcification, not just coronary but just overall vascular calcification.
Speaker 2:And if you think of it this way, you've got different mineral deposition, particularly calcium of course, coming from the calcium hydroxyapatite and we always say from the bones, because that's the main storage site into the vascular system and then going into the vascular wall because it gets trapped. So it's like a big centrifugal force going through the arteries and then it just gets trapped because it's I don't know heavier. It's like a big metal going through and it embeds in the overtime. As you know, we're talking about foam cells, atherosclerosis etc. And it starts that calcium you know process and this deposition also combines phosphates, other minerals I'm going to suggest even heavy metals get involved.
Speaker 2:Um, I had a patient many, many years ago that had an issue where no one could work out what it was and we ended up working out. Long story short, the GP came in with her and it was a very serious case and her files were can't see my hands, but really massively printed out, every test under the sun and I just about you know bone deposition. Everything that we sort of mentioned today and what I found out was due to her childhood. There was different heavy metals in the area and that's what deposited into the tissue and when she moved around, that tissue left because she didn't have enough vitamin d, vitamin k etc. And then left the bone. So she had bone pain and then embedded into her vascular system, leading to cardiovascular risk.
Speaker 2:So that was a good example of someone that had heavy metals as well and metals combined with metals. If we go back to our anions and cations and everything else like that, they all the biochemistry all combines together, leading to this complex which then sat in the arteries and it can sit in the basement membrane of the artery, it can be on the inner or outer side of that membrane, leading to an inflammatory process, an oxidative process, leading to like a firestorm in there. The body tries to heal it by laying down, you know, fibrin and different connective tissue to help protect it, putting a Band-aid down, I suppose. And then that's when you get your atherosclerosis, your plaque formation and then, yeah, your eventual clot in that area yeah, yeah so it's.
Speaker 2:It's a big process. So if we think about that as occurring and then we reverse that process by thinking, okay, we've covered today, thinking about vitamin K2 and how vitamin K2 works with osteocalcin crystal deposition, you know the microcrystalline fibers in the body, and then you've got your cell matrix and hydroxyapatite, we can then start moving and directing, as I said, vitamin K2 to me as a director, directing it to the right place. And it sounds very sort of story-like, but that's the way how a lot of our body works. It's a big story that's been directed by our DNA. The main director, like our genetic code, is telling everything what to do. So if you think about, you know that different process, just with this calcium, you know fortification in the coronary artery and other areas, we can start thinking about vitamin K2 and how that can benefit.
Speaker 2:And there's a lot of different research studies coming out of you know the really longitudinal studies. So these studies have been going on, you know, like the Framingham Heart Study, the Leon Study, the Nurses Study, the Health Practitioner Study, the States Nurses. There's a lot of research studies now where they can look back over test results from the past. There's blood samples from the 1940s and 50s and stuff that they can actually pull out of minus 80 freezers and actually test it for new inflammatory mediators that were never around even 10 years ago. So they're able to do a lot more of this research. And a lot of research is starting to show not with just those kinds of studies but other studies that vitamin K2 depletion over a period of time has led to a higher risk of arterial calcification as well as just general calcification of the body in the wrong areas.
Speaker 1:Yeah, this is one of the areas that interests me in that when looking at the research, some of this negative research was coming out saying that vitamin K2, mk7 did not reduce coronary artery calcium score. But I know, clinically it damn well does. I had an elderly gentleman who had a I mean, you'll fall off your chair when you hear this coronary artery calcium score, a CAC. The CAC was originally something like 5,000. Now I haven't got the things directly in front of me, but it was something in that vicinity, whereas anything over 400 is of clinical like Huge clinical significance 15% risk.
Speaker 1:So this was in the thousands. Upon taking now I'd have to work out the exact dosage. Forgive me, but on taking around about five, six, so let's say 300, forgive me, forgive me 600 micrograms of k2 combined with 6 000 of vitamin d, plus there were some other supplements in there. Because of the health conditions of this gentleman, um, within a six month period, his coronary artery calcium score was reduced by half. Now that's still massive. It's still massive.
Speaker 2:It's still 2,500, but that is a significant reduction in risk. So this person was leaching bone.
Speaker 1:There was a ticking time bomb, and you're right. You're right leaching bone. So it makes me query the quote-unquote evidence where they say no, it didn't, when I've seen it work like that. It definitely does reduce CAC.
Speaker 2:It definitely does. And dose we'll talk about later because I've got a couple of points I want to make. On dose, you know very specifically for what you've led into it very well actually, um, where I'll talk about a couple of clinical cases as well. So what I'll do, I'll finish off this journey and then I'll talk about the reasons why I believe that those doses do work in some cases and don't work in others, because it's sort of, once we have an understanding of you know where this journey is going, you'll see why certain doses work, and that goes with any nutrient, any herb, of course.
Speaker 2:So if we continue through our turbulent journey of our vascular system forging ahead, you've got arterial stiffness as well. So you've got the calcification, you've got the stiffness. Now, thinking about that person you just mentioned, they're turning the stone with that calcium score. It's a very high calcium score, so they're literally turning the stone. So arterial stiffness as well as vascular calcification are very good predictors of cardiovascular and overall health. I'm going to say so. A lot of test results can let us know overall health. So there was a NAPN study which is quite well known. There was a double-blind, placebo-controlled, and I've got to get the number right, I've got it in front 244 healthy postmenopausal women, because you've always got to throw in the healthy part. So healthy typically means that they don't have the condition that they are testing for. So in this case it was 244 healthy postmenopausal women. They investigated the effect of vitamin K2 at 180 micrograms a day, which is a standard dose that we use in Australia. 120 in that and placebo is 124 people for three years. So having any nutritional study for a month is pretty good. Six months is really good. Three years is really really good. So the longer the research studies the better. So after three years they found that K2 improved arterial stiffness, so the artery is more flexible. So sometimes we have to be careful when we say improved, because the word can go both ways. So improved arterial stiffness, especially in those with already high arterial stiffness. So it sounds quite interesting that in the people that already had a high level of arterial stiffness they had a very good improvement in their blood flow and a reduction in arterial stiffness at that dosage of 180, versus what you were mentioning earlier. They seem to have also had a reduction in the GLA protein matrix area that was seen to be having a negative impact. So the flow of calcium in the body was seen to be more improved. So that's just one study. There are quite many more we could talk about but due to time I'm trying to have greater examples of each one.
Speaker 2:If we go from arterial stiffness to a wider range health condition, now called peripheral artery disease or arterial disease. So we've gone from calcification to arterial stiffness. Now we're looking into a disease state name, I suppose, and this is our journey. So peripheral arterial disease or artery disease is actually more common than you think. Arterial disease or artery disease is actually more common than you think. So think of the name peripheral. So legs, arms, hands, feet, you know arterial, just arterial blood flow in disease is just disease, it's just a condition. Base Now what they've realised and worked out with research, again with longitudinal studies, that a low vitamin K2 status has been associated with increased risk of peripheral arterial disease.
Speaker 2:So again, they've been looking at a lot of studies. So here's a little study for you, andrew, sorry about that A 12-year study. So here we go, 12 years on vitamin K2. So this was the intake, measuring the intake on a small number of people, 36,629. So here we go. This is where we want the guts of things now. So this is where we really see some really good research come through.
Speaker 2:At the end of 12 years, vitamin K2 intake was associated with a reduced risk of peripheral arterial disease, with a hazard ratio of 0.71. So what this means for the audience is hazard ratios are quite interesting to look at. If you think about it, if you have a hazard ratio of 1, you're likely to get it it. If you have a hazard ratio of one, you're likely to get it. If you have a hazard ratio of 1.5, you are 50 percent more likely to get it. In this case we are 0.71, meaning there's a 29 because you take that from one, 29 less chance of this happening. So that's the hazard ratio. So I think that's a pretty good number that you know. Your vitamin K2 status over that period of time meant you had a 29% less you know chance of this happening. 10% for me is great, if you know what I mean. Statistically, of course, the higher or in this case, the lower the hazard ratio, the better.
Speaker 2:High blood pressure was measured in this study as well, because I measured a lot of different areas. Hazard ratio was 59, sorry, 0.59. So there wasa 41. Reduction in risk. Type 2 diabetes had a hazard ratio of 0.56. So we're looking at a 44% reduction. So this is just from the humble intake being measured of vitamin K2. So I think it's quite exciting to see a lot of this base research being done. Of course, it's large numbers when we get this. But something very interesting for me, going back to where we first started, the intake of vitamin K1 had no association with reduction of peripheral arterial disease. Right, and why is that? Think back to when we first started.
Speaker 1:It's different molecule length, but yeah. Different molecule length, I mean, but not just molecule length. There's an answer. It brings into question things like methylation as well. That's it On treating an existing condition.
Speaker 2:So the winner of this gets a copy of my book to be published. So this is a question for the audience. You get a prize, but I'll give you the answer as well. So at the beginning, vitamin K1 I mentioned is intrahepatic. It mainly stays inside the liver.
Speaker 2:Vitamin K2 is extrahepatic, meaning it goes out to the tissue. So vitamin K1, for example, in these patients, stayed within the biliary, stayed within the liver system. So therefore it would generally not have an impact on peripheral arterial disease because it's in the periphery, while vitamin k2 floats we'll use the word floats floats around the body on our ldls and chylomicrons and everything else like that. So therefore it's able to achieve its point. So there's a good example of where k2, being extra hepatic, is able to do something at the far ends of the earth, being the hands, feet, legs and arms.
Speaker 2:So goes back to, like I mentioned earlier, structure, function, biochemistry. Every time we need an answer think back. The answer may not be scientifically proven yet, but we start to think back in. What are we thinking about? It's the physiology, the background work. In this case, that's my answer is k2 did the job because it's extra hepatic, it went outside the liver and did its job rather than inside the liver. They didn't do any hepatic markers, which would have been interesting to see, of course, but that's another study to be done. I could yeah, well, andrew, both of us could sit down and write a whole heap of studies about what we'd like to research right now. It's quite exciting.
Speaker 1:Brad, we spoke earlier about doses. We need to cover this off. What doses are appropriate? Can I quickly ask, by the way, that large study that you were talking about before, was that the Rotterdam study, or was that a different one?
Speaker 2:It was a different one and I can't remember the name right now, but it was a different one. No, that's all right.
Speaker 1:They all have different acronyms. That's fine, can we? Cover off on dosages, because one of the things that's interesting me is out of convenience, we tend to combine D3 and K2. Is out of convenience, we tend to combine D3 and K2. But the more I learn about K2, the more I'm wondering about the formulae on the market. Are we wasting the K2? Are we taking not too much, necessarily, but are we just wasting the dose? Should we indeed be taking D3 separate from K2?
Speaker 2:That's a very good clinical point when I was thinking about talking with you about this. Is you know how far do we go? Because I've got notes in my brain on metabolic syndrome, peripheral neuropathy, alzheimer's disease, multiple sclerosis. There's a whole heap of different avenues we can go down to Some of these studies. Are you know, I'm just thinking of one now 625 people over 10 years for metabolic syndrome, type 2 diabetes. There's, you know, a lot of different avenues and some of this sometimes comes down to actual dose.
Speaker 2:So think about the application sports gout, other health conditions. It comes down to actual dose. So think about the application sports gout, other health conditions. It comes down to dose. Now, typically the doses we use here in Australia we are limited with TGA, so therapeutic goods administration on doses of vitamin K2. So appropriate doses, I'd say, is based on the age group. So typically adults are 90 to 180 micrograms per day. Based on the research like the NAPN study and a lot of other research is based on that dosage. 900 to 180 micrograms, sorry, 90, not 900. 90, please. 90 to 180 micrograms per day. Children 10 to 18, because clinically they're seen as children still up until the age of 18, that's 90 micrograms per day. Children 10 to 18, because clinically they're seen as children still up into the age of 18. That's 90 micrograms per day and children less than 10 years of age is 45 micrograms per day.
Speaker 2:So I'll talk about safety avenues in a moment, because that's something that you and I have discussed over coffee about. You know, safety of um, nutrients and nutritional medicine, etc. The reason why I think the doses can be too high is it comes down to metabolism. So it's too much of a good thing is a lot. So you know there's an old saying someone's what is it? Someone's doses, someone's healing and someone's poison. I forget the whole phrase, but there's a phrase of. You know it comes down to the dose of the person and if a lot of research is being based around this 90 to 180 micrograms in in adults, that's that's an area that we seem to really need to sort of focus on and keeping in mind.
Speaker 2:Is it making the pathways work more effectively? Is it, you know, depositing calcium crystals more effectively? It's, it's hard to say because I haven't seen a lot of that toxicology data, for example. But you start to think about how things work. Are we wasting it with? You know, combining k2 and d3? Um, no good. No, it depends on the formula and, of course, the person in front of us, and that's one thing I always want to say when we do podcasts and everything is it's always the person in front of you. What is the best dose for that person? And if they need 500 ius of vitamin d and 90 micrograms of k2 from your determination, that's the dosage that they need. If they need a higher dose of, you know, 1,000 IUs vitamin D3 and 180 micrograms K2, that's the dose regime and that's where a lot of the evidence is showing. So going hard and fast is not always the best way to do it, because to me, it's trying to push too much through all the time. Um, we get excited.
Speaker 2:Some studies are very, very high dose and they seem to have the negative impact because I believe the regulatory pathways are not able to function effectively to make sure we get the best out of you. Know what it is. A good example is water Dehydration. Water is very bad for you, but so is drowning. So if you stick to the 30 mils per kilo body weight per day, that's the NHMRC guidelines for water, for example, or fluids, including tea, coffee and don't get me started on the caffeine argument, because when you have a coffee you're having caffeine with water, so therefore it repletes at the same time. Um, if you think of it that way that's the guidelines based on the evidence then if you start drinking five, six, seven, eight, nine I've seen some people do 10 liters of water a day and they're always feeling sluggish and bloated and feeling bad, it's over hydration. You're drowning the cells with fluid, you're going against the concentration gradient. Sodium, potassium, pump nutrients, electrical impulses are not working effectively and you can get you know fluid in the brain and die of a stroke or something like.
Speaker 2:Let's just go serious for a second.
Speaker 2:That's simple, by changing the dose of water. Now, if we bring that back to a microgram molecule such as vitamin K2, and even D3, it's in micrograms as well. As I use, these are based on doses that the body seems to accept quite well in metabolic studies and seems to do the actions that we need. And I believe that, like with anything, if we smash the body hard, these channels that the body has based on evolution from when we're cave men and cave women and didn't eat every day, and you stored you know nutrients in the body for a period of time and used them as needed, we didn't eat as much as what we do now. We have food available 24 hours a day.
Speaker 2:The body's mechanism of metabolizing and trying to clear excess you know toxins but as well as nutrients is not as functional as what we're pushing in. So that's what concerns me when I see very high doses and some of these studies are actually good for us because then we can see ethically maybe not, but some high dose studies, we can see how well something works. But also get the different thresholds, because if the research showed that you know currently 180 is good, but let's just double it to 360 micrograms is a good dose, we need to then change our guidelines in australia to meet that. But currently, like I, the NAPN study and quite a lot of few studies out there are actually showing that the dosage between 90 to 180 micrograms to adults seems to do the work.
Speaker 1:I take your point and you know I was thinking about the risk of possibly not giving enough credence to other important signals, like inflammatory signals, for instance in cardiovascular disease and calcification. Brad, there was one more thing I just wanted to ask you and that was so maximal dose. We should be really looking at that 180 micrograms, maybe a little bit more, depending on who's in front of you. I get it, but not going way high, not going too high because of those other things. That's right. There was one study I looked at and even though it was a high dose and forgive me, I can't remember the dose there was no risk of extra. Let me word that correctly there was no extra risk of thrombosis. So it wasn't acting like a vitamin K antagonist, if you like.
Speaker 2:And that's something that we discussed recently ourselves, like talking about interactions with pharmaceutical medications, for example. Example, and it does always come down to the person in front of you. You know what medications are they taking, what other vitamins, minerals are they double, triple dosing on things? You know what kind of effect are we looking at and there are a number of um studies that were out there and one of them showed there was a small study that showed 45 micrograms a day decreased the mean value of INR in. Some patients say yeah, inr is related to blood coagulation. So if you think of it that way, a lower INR means the blood clots more rapidly and a longer or higher INR means it takes longer. So that was one study and that's the one that tends to be picked up by people. There's always certain studies. So I always turn around and say read the studies, read the research. You know, understand the person in front of you, look at the genetics, the biochemistry, physiology, etc. And always be careful what you read. Read the full journal article, because the abstracts always look good until you read the full study. I'll give a quick example because I know we're running out of time.
Speaker 2:But there's a big omega-3 study published many, many years ago. That said, omega-3 was really bad. It leads to thrombosis and clots and hemorrhages and will kill you. And I've gone, wow, I did my phd in omega-3. So I'm freaking out now going, wow, what's going on? So I look into it and this was a case study, so I'm going. Okay, case studies are good. It's a level of evidence that we need.
Speaker 2:It was a man in his 70s okay, so he wasn't young. He was admitted to hospital with hemorrhaging and further investigation, which was sort of written in a very small part of the article, was he was outside, fell off a high rung of a ladder, hit the ground, knocked his head and he was taking multiple medications blood pressure, aspirin, warfarin, non-steroidal anti-inflammatories and a whole heap of other things. But it was the omega-3 that caused the hemorrhage. And I'm like really not the fall, not the medications, but the actual omega-3 it did it. So I get a bit triggered sometimes when, um, I sort of read some abstracts where, you know, I believe in all research is useful, but it needs to be factual research.
Speaker 2:And that kind of thing was a bit misleading because the media picked it up and went with that omega-3 causes hemorrhaging when it can if, given the right situation, you're a 70 year old man who fell off a ladder and landed on your head, so therefore there's going to be other consequences of having that, let alone medications. So, yeah, always read the full paper, look into it deeper. So now, after this podcast, go and read up all the material, go and have a look and, you know, nourish your own brain with you know, information of biochemistry and genetics and physiology, because we're learning more and more every day and that's what I love about nutritional medicine, naturopathy and what we do because we are learning more and more and the greater the information coming out. It's fantastic and it's just for me, it's very exciting the time and place we're at right now with what we could do for our patients and help each other out as well.
Speaker 1:Dr Brad McKeown, thank you so much for taking us through. This is a big topic, I know, but vitamin K2, MK7 today it's been great having you on. Thank you so much for joining us.
Speaker 2:Thank you very much for having me.
Speaker 1:And thank you everyone for joining us today. Remember we'll put up as many show notes as we can. There's a lot of research here, and you can find out all of the other podcasts, of course, on the Designs for Health website. Thanks so much for joining us. I'm Andrew Whitfield-Cook. This is Wellness by Designs.