YouTube Video 73 minutes__
Interesting that he is a "world expert", having ZERO Vitamin d publications
His substack
Speaker A
I see it as false hope for people. There's a lot of people that have been looking for a diagnosis of why they're suffering from autoimmune disease or why they're sick, and then they get this vitamin D deficiency label and then they start going down that road and taking a lot of what's really a powerful sacrosteroid hormone and it's going to lead to a bunch of other imbalances in their body.
Speaker B
Shall we walk through the vitamin D sort of pathway? Because a lot of people don't know that there's active D. They don't know you can test for it. They don't know how vitamin D is made and what's the difference between what we make and what we buy in a factory.
Speaker A
People will actually take the d three instead of letting their body make it, and that will leave the 70 hydrocholesterol substrate. There'll be more of it left available to become cholesterol. So taking vitamin D is known to impact the lipid panel in a negative way for that reason right there.
Speaker C
Hello and welcome. I'm Sarah. And today's video is going to be all about vitamin D. And I have one of the world experts on vitamin D as a guest. So Jim Stephenson Junior has been researching vitamin D for over 20 years. He's also published papers on this subject.
Speaker B
And he's regarded as one of the.
Speaker C
World experts in the field. Jim's drive to study vitamin D was after a family member was prescribed a very high dose of vitamin D for osteoporosis. And it turned out that this made her worse and created other complications. This incident gave Jim the incentive to research vitamin D in detail, uncover bad studies, as well as the financial incentives behind vitamin D supplementation. Before I hand you over to Jim, I know based on the topic of this, the vitamin D, I'll get a lot of questions and comments about what to do in northern latitudes such as the UK or Canada and some of the northern states in winter when there isn't UVB to make vitamin D. If you've got enough storage D, this will just convert into active D during the winter. And you'll learn about this when Jim talks about it. At the end of the video, I'll talk a bit more about the chroma D, vitamin D making lamp, the spurti and the krypton, and just show you what they look like. If it's something you already know about, I have experience with all three. And if you want to buy a krypton or a chroma D. The links are in the description and you can use code doctorsarah for a discount. I've also put the link to spur t, but you can buy them in all kinds of retail now, even, I think, in Walmart and on Amazon. So I'll hand you over to Jim and his expertise now.
Speaker B
Welcome to the channel, Jim. I've been really looking forward to talking to you about vitamin D for such a long time. Do you want to introduce yourself to everybody and let them know what we're going to be talking about today?
Speaker A
Sure. My name is Jim Stevenson and I've been researching vitamin D for it'll be 20 years next year because somebody was diagnosed with a deficiency and almost everything that was wrong with them was blamed on that deficiency. Deficiency. And that's what you see in mainstream is that it's the one thing that we might as well call vitamin D deficiency a syndrome because they want to link everything to it. There's not going to be a paper on most autoimmune diseases where they haven't measured vitamin D and try to blame it low level based upon the goal they've set for what's wrong with the people. And it's just not realistic because they're measuring an inactive molecule of which there's several different forms. And so it's, it's just, uh, I, I see it as false hope for people. There's a lot of people that have been looking for a diagnosis of why they're suffering from autoimmune disease or why they're sick, and then they get this vitamin D deficiency label and then they start going down that road and taking a lot of what's really a powerful sacosteroid hormone and it's going to lead to a bunch of other imbalances in their body. And it's in studies. Clearly, it's nothing working to fix people. They're getting hope from association based studies that look at the past and say this level of vitamin D led to this disease condition, but it won't reverse it, it won't correct it, but that's what's driving the hope and causing the people to take the vitamin D in the first place.
Speaker B
So with these studies, has anybody ever thought to just ask how much outdoor time they get? Or is there something going on in the background? Because obviously a vitamin D supplementation is a big business, same as any supplement business. So is it bad science or is it financially driven?
Speaker A
Well, they try to look at that. The problem with when we go in the sun is that they've created the science to look like when you make a certain amount of vitamin D three, and then the rest just goes on and progresses to an inert substance, which isn't true. It progresses to a substance, can revert back to d three, and then has a whole family, as I say, of molecules that actually do things, even though they don't act on calcium, which is what got their inert label in the first place, just because they don't mobilize calcium. And I think a lot of people know now that the active form of vitamin D can really get them in trouble with calcium. So you want to be really careful with it. We wanted some of these other molecules that were abandoned as inert because they didn't mobilize calcium. And when you research those molecules, you'll find that they actually do a lot of wonderful things. So it's just those are the drugs that are being. They're making clones of them pretty much, and treating the autoimmune diseases with them. And you can find that literature if you know what to look for.
Speaker B
Okay, shall we walk through the vitamin D sort of pathway? Because a lot of people don't know that there's active d. They don't know you can test for it. They don't know how vitamin D is made. And what's the difference between what we make and what we buy in a factory?
Speaker A
Okay, sure. We can start with the substrate that would make the vitamin D three naturally in your body when you go in the sun. And it's a form of cholesterol, and it's what cholesterol is made from. Two, it's called seven, dehydrocholesterol. So the sun will act on that, the uvb range of uv light will act on that and alter that through a couple small steps to where it will actually become what we know is d three. People will actually take the d three instead of letting their body make it, and that will leave the 70 hydrocholesterol substrate, there'll be more of it left available to become cholesterol. So taking vitamin D is known to impact the lipid panel in a negative way for that reason right there. So once you have d three, whether you ingested it from a pill or made it in the sun, it's going to travel through the body, but it's going to travel in a completely different way if you made it in the sun than if you ingested it and it went into the gut. If you make it in the sun, it will be transported by its carrier protein, which is vitamin D binding protein. And that will take it to the liver. Your gut will also pick it up using LDL cholesterol, which is another impact to your lipid panel, because LDL cholesterol can easily get you flagged and headed towards a statin treatment. So then the LDL cholesterol will shuttle the d three from the gut to the liver. And at that point, the liver will turn it into what they measure, which is 25 hydroxy D. Hydroxy vitamin D. And we're talking right now, we're talking about the d three faction. You could ingest a d two faction, and it would be carried from the gut in the same manner with the same LDL cholesterol. Go to the liver, and then be activated to a d two form of 25 D. From there, it leaves the liver headed to the kidneys to be altered to the active form. That journey right there is where things get measured. So you have to keep in mind, the liver had to make the decision to release the 25 d into the blood that they're measuring the first place. So it's in control of how much is in there. Your body's in control of how much is in there. You can take a lot of vitamin D and push a certain amount through. Some people can. Some people's body has a real problem with that, and they can take a ton and hardly even see a change in their vitamin D. So that active form made by the kidneys is the one that works with the RXR receptor and vitamin a to make what I call the chemical and biological warriors, your immune response. That's the molecule of immune response that makes the things that the body decided it wanted.
Speaker B
Okay. Yeah, that's really important, because when I talk to people about vitamin D, I just try to simplify it and say storage D and active d. So what you've said is somebody could be hoarding a huge amount of storage D in their muscles or their liver. And because it's a storage molecule, it shouldn't really be in the blood anyway, unless it's doing something. So straight away, measuring just storage D would look like quite a bad marker, just regardless of having an active form, that for some people it might be in the blood, some people it might be in the liver, and you could have organs full of storage D. And then are people taking supplements on top? And we don't know what happens next, because what happens if somebody, say, thought they had, they had pseudo low storage d and they took a huge amount of d supplements, but there was already a lot of vitamin D in their livers? And their muscles. What could be some of the side effects of these supplements?
Speaker A
You're always messing with calcium when you're talking about d, 325 D and 125 D, what we call the vitamin, the storage in the active form, because if you get enough of any one of those in you, it will spike your need for calcium in blood. And when your body has a need for calcium in blood, it's going to find it and it's going to put it there. And if it finds it in the gut, that's still a lot of work for the body, but that's a lot different than if it has to go to bone to get it. And then you're going to end up with. With osteoporosis, a human form of non fatal rodenticide, as I call it.
Speaker B
Okay, that's pretty serious because, yeah, osteoporosis is massively on the rise. And you mentioned earlier that DNA pair together. What happens to the retinal, the vitamin a, when there's far too much d? What kind of effects could that have on a person?
Speaker A
Well, I do know that some of the literature talks about how the two compete for absorption. So you have that to begin with if you have a need for it. So if you were taking them together, you might not get or eating them together, which is the much better way to get it. They might compete for absorption, and that could be an issue for you. And they're both fat solubles, so they're going to both be acquired in the same fashion with the LDL cholesterol and things like that. So. And there's a lot of different forms of vitamin A, and the literature's changed over time. Right now, the form that we say works in the RXR would be called vitamin a five. I think that paper was written in 2016, so there's a little bit of controversy of which vitamin A molecule is doing the work. But I wanted to talk for a second more about that 25 D marker that they're measuring. In my research, I found 15 different forms of 25 d. And I've also found that in certain disease states, you will start to make different forms that they aren't measuring traditionally. And so the ratio of vitamin D that they're looking for, they might only be picking up half of the two 5d molecules in your blood and labeling you deficient because your body's making one that isn't influenced in calcium. We see this in children, we see this in diabetes, other things like that. The body is going to make a conscious decision to make molecules that don't influence calcium when it doesn't have a need for calcium. So that's pretty important to recognize.
Speaker B
Okay, so what. What else do you know about these other forms of vitamin D? Of what else do they do?
Speaker A
Well, they. They haven't really nailed down what the epimerization form one does. There's a sulfated, a water soluble form of it, and then there's a fat soluble form of it as well. What they do see is that when you supplement the children with it, they will have up to 60% of their blood in the epimerization form that the papers I've read didn't differentiate between that and a sulfated form. I think that was just pointing to the fat soluble form, but it was up to 60% of their blood to five daughter. And they're being labeled deficient and being told to take more of your traditional d three.
Speaker B
And when they were labeled deficient, did anybody measure their active d, the 125 dihydroxy, or did they just do it purely on the storage d?
Speaker A
They just do it solely on the storage d. You pretty much have to ask in demand for a 125 d test. And in the United States, there pretty much trained to not test that. So we don't have a whole lot of data out there or data sets that show how it is in conditions and in disease states. They just aren't measuring it. We know it's going to be high in granulomatous diseases like cancer, sarcoidosis. I think it's going to be typically high in almost any disease state. Therefore, what is the big question at the end of the day would be, what do the people think that more vitamin D is for? If the molecule that's active, that's doing the work is already high. So that's the big question at the end of the day. We know there's a lot of people that are wanting to raise their vitamin d level, their 25 d level, because of the association based studies showing people with lower have all these diseases. But there's no literature showing what would be the mechanism if it were to work, which it's not working in the studies. But if it worked in the studies, what mechanism are they watching for to actually do the work? If we could go a few more decades just measuring two, playing games with associations and disease states. But that's not getting anybody anywhere.
Speaker B
Yeah, exactly. So if we loop back to the active form, the 125 hydroxy, I measured it using quest because they freeze the sample, and then when it comes to understanding ranges and what it should be, I think from following you for a while, is the active d meant to be twice the storage d, or about one to one or one to three? But then if you see a really low storage d and like something like eleven or seven times more active d, that's sort of showing a disease state, because some people might have both results and then they don't know what the. They have active d and storage d tests, but then they don't know what they should be looking for and what's good and what's bad when they've got the correct tests.
Speaker A
Right? Well, first of all, it's good to just look at the 125 D test by itself and just think about where it is in its range. Is it in range? There are a lot of people that is actually above the top end of the range. I've never. I've seen two peoples level out of range low, and one had hypoparathyroidism and the other one had chronic kidney disease. So they both had defects making the active form of vitamin D. Other than that, I've never had anyone give me a lab that was low. I think with one exception, another person who shared a lab, and it was also a hypoparathyroid situation. And these people take the active form of d because they need to have it. It's super important to have it. So outside of that, I haven't seen it low. So you start there. When it comes to assessing the 25 D number, you have to take a couple things into consideration. The season for the person. And how drastic is that season where they live, sometimes it's just a little tiny dip, other places it's a huge change. And what were they doing? What is influencing their number already? Have they taken vitamin D in the past? Is it still part of that number for them? So you have to take all that into consideration. But when you have someone like you just said, where they have seven times as much active d as the storage d, say like the person I began with, it was eleven and 76. When you have those, that's what I call a dysregulation. And their papers written about that high 125 D, coupled with low two 5d, there's exactly that paper written. And that those are the kind of people that help drive that full self fulfilling prophecy where they think that the higher your level, the better. Let's imagine that person with eleven and 76 is in a study on the big C disease that we just went through, or still going through if they're in a group. And that person, keep in mind that person started at 23 before they took the dose, the 50,000 rx, that's what dropped them to eleven. Imagine that person went into a study and it was going to be a bolus dose, just like a prescription. And you give all those people the vitamin D that person's dropped. Some people's won't rise at all. But then there's the healthier people that aren't already having a lower two 5d that will go up and they'll credit all the good things with that 25 d number. Driving home the higher number is better. But the reason that the two 5d is higher in healthier people is because it's a negative acute phase reactant. That's super important to understand. C reactive protein is a positive acute phase reactant. It's going to rise in diseased people, in sick people, people with inflammation. Well, the counter is true of the 25 D. It's going to drop in people that are sick. It's a marker for illness, just like C reactive protein is marker for illness. They just go in different directions. So 25 D should be expected to be low in sick people. It's a marker, not the cause. They're not burning through their vitamin D. It's not getting used up in the form of 125 D. That's not what is happening. The literature shows that those two molecules are not connected like that. They, you know, they just don't correlate like that. So that isn't the situation. But to make, to drive it home even worse is that the carrier protein, vitamin D binding protein and albumin, which 15% of albumin carries around 25 D, both of those are negative acute phase reactants. So you have a triple hit to that system right there. So you should absolutely expect it to be low. And there's papers about this specifically saying that's why it's low with the C disease, the c virus.
Speaker B
Oh, okay. Okay, I see, yeah. So when it comes to what people should do next, say if someone's listening and they're getting ready for winter and thinking, oh no, I live in Canada or the UK, I need to start supplementing. Should they be checking their active d all the time? Because that should stay the same all year round, is that correct? And then the storage d will fluctuate just because in winter people are just using up their storage so there's no need to get in a big panic. What would you say about people entering in winter? And there's obviously, I won't mention names of influencers who are really hammering home, taking vitamin D and then doctors will. I was reading some labs yesterday, and it even says in the vitamin D section, it tells people to supplement, whether they're, it was a UK lab, whether they're deficient or not. So maybe if we talk about how these levels change through the year and how not to get into a panic about winter and not to panic if your storage d goes down during winter.
Speaker A
Right, you should expect your storage d, as they call it, to go down during winter because it has a seasonal variation, because the d three, which a certain amount of it's always going to progress through, whether you're taking it or making it into the sun, to two. So when there's no uvb in the winter and you're not making d three, it's naturally going to see the seasonal variation where it drops, whereas the active form of vitamin D, the one that does the work, the goal, it doesn't have a seasonal variation. And this is where people need to really stop, disconnect for a second and think, we get sick in winter. In general, we get sick in winter. There's a couple exceptions. Polio was an exception. It was a June July disease. But other than that, we get sick in winter. It's tied to people moving from certain geographic locations because of school quarters, semesters, and absolute humidity and things like that. But we get sick in winter. If our immune system were so pathetic that it actually took the winter off when we were going to get sick, we wouldn't be here talking today. We wouldn't be a species that even existed anymore. We would have perished eons ago, the first few winters we went through. So that's not how an immune system works. It would be a defective immune system that worked that way. And there's papers about this showing that there's no seasonal variation in that. And even if it, even if you were concerned about lower two 5D, there are papers that show that people are able to pull 30, 00, 40, 00, 50, 00 IU out of storage every single day during winter.
Speaker B
Okay, where do they pull it out of storage? Is it fat and the muscle, or where would it come from?
Speaker A
They didn't have it labeled, so they just, they choose that. It probably comes from abundance of all those sources. And the chief storage organ is the liver, though, and so the vast majority of it would come from there. It's a real disservice to us for them not to have figured out a way to test that there, or to actually be following in all these studies what molecule it's becoming that would be hopeful to make things better for everybody. Nobody's looking at that. We're just so obsessed with association based science that sells more pills and tests of vitamin D, and nobody's getting well. And we have study after study that says we need a new study.
Speaker B
I was just about to ask you, in a perfect world, in the vitamin D world, what studies would you love to see done? What do you think are the three most important ones that should be set up and performed?
Speaker A
Well, I think that if. I think you would want to probably go ahead and look at what's gone on with the MS patients who have taken really, really huge doses and try to pick a few case studies that you think it really worked on, and then use them as an example and do some radio labeled molecules, see where they go and what they become and see what's going on with that, because a lot of people feel hope in that. Ms. Cambrio, I don't know if I'm saying it right, that world from Brazil. So that's a big one. That causes people to think that they can take a ton of vitamin D. And if you read his research, he says that he feels those people have an insensitivity to vitamin D. It's not for the general population, but people do hold up huge doses from the MS treatments, as if just anybody should go ahead and give that a shot.
Speaker B
All right. Okay. So it would be like radio labeling in a situation where a massive dose of supplements on a serious disease really helped people. People and find out what happened. Would you also look at the people in that MS study that the supplementation made them worse? Because there must have been.
Speaker A
Yeah, you'd want to see what molecules they were making them and stuff. And I don't. A lot of people might know this. When you go on those miss protocols and stuff, they super limit the calcium and stuff like that so that they don't get hurt by inputs of calcium. But you need to look at what's going on with their internal calcium, what's going on with their bone. Are they shuffling calcium around, stuff like that? There's not a whole lot of information. I haven't been able to find a whole lot of information about the scientific pathogenesis model that's being portrayed there.
Speaker B
Okay. Because back to what you said earlier about sometimes people just take things and they don't know what they're doing and why they're doing it, because I have seen a variety of cancer protocols and cancer studies where they're adamant that the vitamin D supplementation is vital for this. What's your thoughts on these studies and what those data, most of the types.
Speaker A
Of cancer, I'm sure that if you dig into the deep science of it, you'll find they have a way of blocking the action of vitamin D. They wouldn't express as many vitamin D receptors as they do if vitamin D was going to go there and kill them. They express up to 400% more vitamin D receptors than healthy tissue adjacent to the tumors. And so if vitamin D was going to go there and kill them, that would. You'd see it immediately. Others, they cease to express the vitamin D receptors. Each cancer model is different, and there's different forms of cancer inside each model, actually. So that's pretty complex, but it's not working. They run into hypercalcemia almost immediately, trying to use a one two 5d molecule or one like that, that influences calcium. But the sad thing is that you can follow other pathways. Here's the difference. If the science is coming to you in your inbox and it's about the vitamin D deficiency, it's going to be fluff. But if you go out and you look at an image of the metabolism of vitamin D and pick a molecule you haven't heard of, and you go and do guided research into it and look that molecule up on pubmed or any of the journals, all of a sudden you may find, wow, this thing cures cancer. Why are we not using it instead of trying to make one like 125 d that doesn't cause calcium issues? Well, because that was a natural molecule, it's not patentable, so they're not going to do it. They'll try to make something like it, and there's probably something like it already. So that's the sad thing. We know which molecules will work that are natural on most of the cancers. We know which molecules that are work that are natural on Covid and some of them are vitamin D molecules, some of them are in honey, but they're not made from two 5d. That's the bad thing. We're so focused on two 5d that we've already committed to a pathway that we know is going to lead to hypercalcemia and isn't working. It's a failed model, in my opinion.
Speaker B
So do you think for some people it's a placebo effect when they take these supplements? Because I've heard people say things like, oh, yeah, if I don't take my vitamin D supplements up, my joints get inflamed. Is there a possible reason for that? Or do you think some of these things are placebo or do you think a lot of the use of vitamin D supplementation is just blindly like, people have got no idea what they're doing, or do you think, I'm trying to even think now of if you ask somebody, why do you take it? Would you feel any different that they tend to not answer, whereas that example of that person who said, oh, no, it helps my inflammation, is that possible that the supplement could do that?
Speaker A
It can do that. It absolutely can do that. We see that in the chemo trials. People probably tired of hearing me say that you give the placebo and they expect their hair to fall out, and 65% of the time it falls out. But this is a different kind of placebo effect because they're getting the anticipated negative thing and they bring it to them. In the placebo effect, they could anticipate the positive thing that that chemo is going to work, whether it should or not, and then the chemo could work. So now let's think about in the vitamin D is helping them world. They're expecting it to help. They're thinking the positive side of things. They're not expecting the negative side of things. So when I see people that are gung ho about it, and I don't mean that to be a negative thing, it seems to help those people that buy in from the get go at least a little bit, it seems like. Whereas other people that are just like, well, I don't know, I'll try it. Those are sometimes the people that are reporting the negative side effects or not. Anything at all. No effect at all. So I think how they go into it in the first place, you're going to either embrace a placebo effect. There's other things, there's other biological things that could be going on. You could be having a steroid effect, like prednisone, something like that. You could be blocking another system that was doing something good. I mentioned this yesterday, doing something good that was causing you to feel ill as you had a pathogen die off or something like that. And once you block that, you're not going to be experiencing the negative aspects of recovery, as they call Herxheimer type reactions. So it could be any number of things, but unless and until they start tracking the molecules, we won't know. We track the molecules early on. I don't know why we pretend like we're in the Stone Age now, and it's just be so complex to figure out what's really going on. It's almost like we don't want to.
Speaker B
Yeah, that's why I was. Because the vitamin D business is too well established now, and like you said, they don't, they're a cancer preventing or helping D derivatives. But like you said, they can't be patented, so there's no money. So people are not interested. Just back again to other effects people report or it's touted with supplements. How does it influence appetite?
Speaker A
You know, I, there's not a whole lot of literature on that. You have to be really careful what you read in a paper that they say is driven by low vitamin D. That's an association because you can just about get anything into a paper now, you know, joke about a bad haircut and stuff like that. I've seen where they said it helped. They say it helps just about anything if they, they study it like that. But it doesn't fix a disease state, or at least they'll say low in it contributes to everything. It's, it's like if you're going to study fibromyalgia, you're going to measure vitamin D and you're going to say its impact on fibromyalgia. If you're going to study Parkinson's, you're going to measure vitamin D and you're going to say, oh, the people do worse this, but that's because it's a marker for illness once again. But it drives home that self fulfilling prophecy. But if you were measuring the 125 D, you'd see that they aren't coupled. It's not low. If 125 D, the active form, were the driver of illness, being low were the driver of illness, its goal would have had to been raised in 2010 along with the goal for 25 D. That doesnt make any sense. We only raised the goal for 25 D. We didnt raise, because you just.
Speaker B
Said previously that really high active D is also a disease state marker. So trying to say more is better isn't appropriate.
Speaker A
No, it isn't. It isn't. It's your immune response molecule. That's why they have that kind of range. And you see a lot of people in the forties. I seldom, seldom see anybody dip below the forties. You know, 40 somewhere in the forties seems to be a really good number to me. That's what I see with people that are doing good. You can see with people that aren't doing good too sometimes.
Speaker B
Oh, right. So that's in the forties for the active 125 D. Correct. Because also the other big issue is there's a big massive debate about what the storage D should be. And there's a little bit of sort of where did this number come from? Maybe if you want to talk a little bit about what? Because we've talked about low D, what's classed as low, and is it actually not the wrong range?
Speaker A
What it is, is they used to have a goal, and I think I've said twelve and a half a lot, but I think the goal actually originally was ten to 30, you know, but ten being the bottom end, and they wanted to move it to 20, and that's actually what they set it at. Around 2008, the Institutes of Medicine, the New York Academy of Sciences, looked at all of the research and then they came up with a number. And then Hollik followed up with the Endocrine Society and they actually said there was some mistake, statistical mistake, and there wasn't, and got it raised to 30 plus. And that's where we're at now. So if you're below 20, you're going to get labeled deficient, and that would be 50 in nanomole. So 20 is in the ng, and then if you were 20 to 30 is insufficient. And so that's 30 is 60, I believe, nanomole. And if you're above that, it's okay. But some places they're shooting for 40 plus, 50 plus, 80 plus, try to hit 100. So there's a lot of people shooting for higher than that. And so that's all based upon associations looking at who has what type of disease and at what level, what's the highest level? We see those people with that disease and we'll call that the cutoff. And make sure you're above that two 5d number for colorectal cancer, make sure you're above that for Parkinson's, make sure you're above that for lung cancer. So it's all association based. We have no idea what those people's 125 d was, their cancer. It would be probably triple digits. So what is more vitamin D going to do for those people?
Speaker B
Yeah, exactly. Because there's too much data on one form and hardly any on the active form.
Speaker C
Because.
Speaker B
Yeah, just because when you were describing the numbers, I think you went in because our units are in nanomolar and then you were saying that the bars moved. So it's now 20 to 30 nanograms would be all right. And now they're trying to get people, they're trying to say, oh, it should be up to sort of 80 nanograms. I think that's something like 250 nanomolar. So what's going to be the outcome? Or how is this going to do you think it's going to get worse, that this vitamin D obsession is going to get worse and people are just going to be taking higher and higher supplements. Where do you see this going? Or do you think there'll be some kind of study or data coming out to put an end to this? Or will it just keep getting worse?
Speaker C
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Speaker A
I think because of the self fulfilling prophecy piece of it, it's really tough because they're all publishing the same science that's all association based and no one's if you're going to build your whole paper around a deficiency, you're not going to bring a bunch of labs in where those people that you're labeling deficient have sky high active vitamin D and put that in your paper too. I don't think you get published, but it just doesn't make any sense in a deficiency, especially if it's a paper that begins explaining how vitamin D works. Almost every paper on vitamin D deficiency will actually start out telling you how the vitamin D accomplishes what it does. It'll mention the active form, sometimes it'll mention how it works heterodimerized with the Rxrhe. But at some point it will point out this is the one that does it. And then they bait and switch back to a low 25 D and then they don't ever go back and say well we already told you this is the one that's going to do the work and they'll never establish its low and it's not going to be, that's really not compatible with life. You know, you're not going to find a. It's just not compatible with life. You have to have that form of vitamin D and you're not going to be low in it. It, and I've talked about this before, I want to mention this, it's the level of, let's say you go to the doctor and your vitamin D is 20. When the doctor in our numbers in g, the doctor's going to want you at 30 at a minimum. So let's say you start taking an amount of vitamin D 2000 IU every day and that gets you to 40. And now you're at 40 and that's exactly what they want to see. You were deficient, we prescribed a fix. You're in this range, we're happy with you. But the point really is that that doesn't show any utilization of vitamin D. And the reason I say that is because if the doctor's trying to tell you that 20 to 40 that you have in your body now you're actually using and it's making your life better and it's fixing something, well when you take it back away, you drop to 20. If your body needs 20 in G of vitamin D and you take it away, it's going to use the base 20 up and you're going to be at zero. It's just, it's just throughput. That's all you're seeing is throughput of daily inputs of vitamin D. That's why they don't like bolus dosing. It really messes up the consistency of labs because it's all let go at once and the body does it a little different. So you're really not seeing your body utilize any of that 25 d. If you're able to up your lab just from taking it every day, that's not utilization. They could track it, they could radio label it, they could watch what it becomes. They could see that it actually does something. But by and large it's probably just leaving your body.
Speaker B
Okay, so just to summarize what we've talked about, if people read a paper on vitamin D. It's just going to tell you that there's two forms. Briefly mention the active form, and then when you look at the results, all they've done is measured the storage form and pretended the active one doesn't exist and attribute all of anything to that number going up. Then, secondly, all of the people that do this research all kind of know each other. So there's like a group of people, it's like they're publishing to agree with each other. And anything that comes in, like you said, that's going to massively disagree with this, such as looking at active d, they just throw. They kind of throw that data away because it doesn't agree with the narrative. And then you were saying that the doctor might give somebody vitamin D to push it up from 20 nanograms to 40, but that patient might feel no different from being at 40 to 20. And then they take the supplement away and the patient's number goes back down to 20 and the patient still feels exactly the same. So is that sort of how this bizarre vitamin D narrative is working?
Speaker A
Right, but there'll be ones that go to their doctor that won't look at it like I do, and they'll think it's a wonderful thing, hey, I'm deficient in vitamin D. They go home, they tell their family, and they may even get everybody in their family on it. That's a pretty common thing. When people find vitamin D, they want to spread the joy with their family and friends. And it's just. It's not a real thing. It's not. I do think there's one thing that might change this, and that's the fact that we have been ignoring the true storage form of vitamin D for a long time, which is a sulfated, water soluble form. And that's what I've. I went and did a deep dive on and found right at 50, a little under 50 papers on it across a little over 60 years. And that's a big deal, but that's a lot to get your head around, I think.
Speaker B
I wanted to ask about sulfated vitamin D because there's a whole different story to this, because it's like sulfated cholesterol and DheA's, which is Dhea sulfate, but they're kind of a completely different molecule because being water soluble and they have different properties. So you're welcome to talk about some sulfated D because I know that sunlight plays a role in sulfation, but then there's going to be more to the story. But I think it's important to educate people about this form as well.
Speaker A
Sure. Now, I did run into them talking about the DHEA and the estrogen and the other sulfated forms of steroids. And the literature did say that it's commonly known that steroids are stored in a stable sulfated form, ready to become the form they need unsulfated to do the processes they're there for. What I, what I found really fascinating about vitamin D was that the body sulfates, if you could look at the mainstream focus of vitamin D as a four step process, that being 70 hydrocholesterol d. Three, two, five. Djdehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehehe and one, two 5d. There's a sulfated form of every one of those molecules and a fat soluble form of every one of those molecules, not just at one level. Is there a sulfated vitamin D at every one of those levels. And the literature says that the 7d hydrocholesterol sulfate is made from the unsulfated, the fat soluble form. They say that at each level they're made from their own counterpart, and then they return to their counterpart as needed. But what was really interesting about this, the minute you mention water soluble vitamins to people, they're going to say, well, they leave your body immediately. But that isn't true of these water soluble sulfated molecules. I don't know about dhea and the others, but the exact same carrier protein that carries around the fat soluble vitamin D molecules carries around the sulfated water soluble molecules. In fact, the attraction to the carrier protein is identical. So there's no competition for carriers here. And if people don't know it, that's what establishes the half life on those molecules, is the vitamin D binding protein, not the molecule of vitamin D. So they have the same half life now, too, as well.
Speaker B
All right, that's so with a sulfated form, if you do a blood test, can it tell the difference between, or does it detect, does it not detect the sulfated form, or does it get mixed in with the reading?
Speaker A
No, it doesn't detect it. You have to get a specific test. And this is stuff that isn't really available to us yet. I did have one person in my vitamin D group that had a test that they had been two tests. They had been asking us about their two, two 5d tests. And at the time, I was really busy when I finished this research, and I had read about all these new types of tests that do eight and twelve different molecules, sulfated, non sulfated. I took a look at what she had there, and lo and behold, she had a fat soluble two 5d test and a water soluble two. 5d test. Now let's imagine this was the United States and all they got was a fat soluble vitamin D test. This person's vitamin D, fat soluble was eleven. That person would be on a 50,000 IU prescription, immediately dousing their body with fat soluble molecule. What was this person's water soluble vitamin D level? 90. 90. So overall they were 101. They definitely were not deficient. So that's probably what we're going to see. That's, you see breast milk profiles that the water soluble dominates, totally dominates, like 95% to 5% in breastmilk. In all the human serum profiles, whether you're pregnant or not, you're male, female, child, adult. There's more water soluble in everybody than there is fat soluble in the same counterpart molecule.
Speaker B
Yeah, because this is massive now, because people who are cottoning onto things now get d and active d tests. But now we're saying actually that that's not good enough. We need really the sulfated forms if they're the predominant dominant forms. So is there anything else to say about the breast milk and the sulfated forms and carrying on on this conversation?
Speaker A
These two things are really huge. Besides the carrier protein is the fact that supplementing does not alter your sulfated levels. So they're not going to be able to push that narrative that, oh, well, let's at least get. Maybe you get both your levels up by taking vitamin D. No, it doesn't get your water soluble up because that body's already seen that as the storage form to become the fat soluble. There's no seasonal variation in it either. So those two huge.
Speaker B
Okay, because there could be people that have low storage, low active, but then they've got huge amounts of sulfated that nobody ever measures that are perfectly healthy and galloping about. Because I've seen that and there was nothing wrong with a person. Because that's why I was asking you about what studies would you love to see? And I think looking at the sulfated form of vitamin D would be really fascinating.
Speaker A
Right? Yeah. They're going to need to track that through and see, since it doesn't have a seasonal variation, the active form doesn't have a seasonal variation. That's probably the system that's maintaining you through through winter. You're clearly not low in either one of those important molecules. And again, you're not out of vitamin D. People act like 20 is out. I just, I don't understand. It's all association based. 20 people at a level of 20 didn't do as well as people that had a level of 40, just association. But what was their active vitamin D? I bet you the people that had the 20 storage D had higher active d than the people at 40. They're sick, they're going through something, you know, we would expect them to do, do worse. We just need to uncouple blaming that vitamin D for it.
Speaker B
So are you saying that there could be completely. There are other factors totally separate to the vitamin D making them sick or do you think there is something to it? We're just looking the wrong way and at the wrong molecules and we don't looking at the wrong ratio. It's a mixture of both. Both that there's something huge to the vitamin D, but we're looking at the wrong thing. Plus these people might. There might be some other pathway that's making them sick. And it's nothing to do with vitamin D at all.
Speaker A
Right. It could be enzyme competition. If you're on a prescription drug of any kind, the first thing you're going to have to do is rule that out. See how that's assimilated by your body. See if you can read a lot of good stuff about all the enzymes. It's pretty easy to read up on them and see what blocks them, what increases them, decreases them, including the natural things. And you might be on two things that are using the same enzyme and they may be competing with a natural enzyme. So you got to consider what unnatural things you're doing first and rule those things out. But I think we're just looking at the wrong molecules. But I don't know why the body isn't by and large, making the right molecules in the sick people. I can't. I can't say they got blocked in the first place by vitamin D. I can't blame that. I think everybody has the potential to have a different type of hack, as I call it, in them. You know, that's why I say, look at your prescription drug. Is it blocking something? I really don't know. I wish somebody would start radio labeling these molecules and so we could see in the well, people what pathways are being utilized. You can find a lot of interesting stuff, but not utilization. You can find which tissues express this. You can look at protein atlases, you can see the potential for wellness, but they need to figure out why it's not happening. And that's what nobody's trying to do. They just want to tell everybody why they're sick.
Speaker B
But also, isn't magnesium involved in pretty much every step of this vitamin D pathway. So do you think people having different levels of magnesium is part of this story as well?
Speaker A
Some people, if they're truly deficient in magnesium, that could be an issue. I've seen the diagrams that show you where magnesium is used in the vitamin D activation steps. I don't know which molecule it's pointing to in magnesium because there's a lot of different molecules of magnesium. And that gets pretty complicated too. But any of the cofactors could be an issue. It's really like we're not getting, we're being fed association science right now instead of real science. If they would do real science, then we would probably have some answers to those things. But I can say this, though, when I find a molecule, like yesterday I mentioned a molecule that does wonders in the body. When I find a molecule, I look at it, and they have specifically looked at that molecule. They're able to accomplish stuff with those molecules and they're natural molecules. So we need to find out why they're not in us and doing what they do in the studies.
Speaker B
Yeah, that's what I was interested in of what's stopping the right molecules being made. Because you mentioned different medications, medications and drugs. Are there any common ones or classic vitamin D disrupting medications or substances that people need to know about?
Speaker A
Glyphosate messes with Cyp enzymes for sure, in any of the steroid world, including the vitamin D world. I do know that one of those water soluble two five ds that I found is called a gluconeride. I'm probably saying it wrong, but it travels in bile back into the gut. And it's the two 5d arrival in the gut in case the body wants 125 d in the gut. Well, it's also a substrate to make some molecules to go through the body and immediately found out that those transporters are, are used by the statins. And so I think a statins immediately, I think taking vitamin D can easily get you on a statin right away way because its going to mess up your lipid panel and youre definitely going to have more ldl cholesterol to shuttle the oral d you're taking. And then once you get a statin in you, theyre really just molecules of vitamin D. Grimes, David Grimes has done a lot of work on that. And they all have a different, theres a lot of different statins. They all have different affinities to the thyroid receptors, just like vitamin D does. So once youre on any of those meds, and it does look like I'm sure. That if the statins are using, the transporters are called oat. I think it's organic anion. I don't know what the middle word is, but those are the transporters that are being stolen by statins that the gluconeride would make would be a substrate for. So now think about that. There's nothing organic about statins. Why are they hitching a ride on your organic transporters? And those things take things to tumors and stuff like that. So that could be a serious blockage right there. What if the substrate of gluconuride is going to make an anti cancer vitamin D molecule? But statins stole the transport?
Speaker B
Okay. Yeah, that would make a lot of sense. So that, are there any other ones that you know of or any substances like that people use recreationally that might mess up their vitamin, vitamin D? Because you mentioned glyphosate as a sort of like household product.
Speaker A
Well, I do know that caffeine causes you to cease to express your vitamin D receptors in a dose dependent fashion, which makes sense if you look at it as an insecticide made by plants. So it might have a way of blocking our body from expressing vdrs to detox it. That's a pretty simple one right there. There's probably going to be other things like that. I found that paper really fascinating.
Speaker B
Yeah, that's the kind of thing I'm really interested in because lots of psychoactive things in plants are not for us, it's to repel the insects. So yeah, that's interesting because also you mentioned something else that reminded me of a question because you were talking about how the vitamin D and the thyroid receptor have a relationship. But also doesn't the melatonin receptor and vitamin D have a relationship about molecules that can go into other molecules, receptors or dimerization of different receptors? Maybe if we talk about that a little bit because that was really interesting what you said about the thyroid.
Speaker A
Yes. So that's an Amy, I don't know how to say her last name. Proel P r o a l. She has a paper that talks about the attraction of the active form of vitamin D to several of the other nuclear receptors and it always has a higher attraction to the other receptors, which is odd but its tight regulation would explain that. But the minute thats gone youll lose your thyroid to it. Things like that. But other natural molecules. Lets talk about Epstein Barr for a second. Epstein Barr makes three antigens, ebna one, two and three. All of those are the right shape to sit in. The vitamin D receptor but having a flare of epstein Barr will cause active d to be created in your body. So now it won't have its receptor. That's a perfect time for it to go and take the thyroid, glucocorticoid, adrenal, any of those other receptors. So that's a displacement right there. That can happen.
Speaker B
Oh, I see. So. So that's part of when people have really high active d of why they're sick. It's because the active D is going into receptors that belong to a different ligand and then creating.
Speaker A
Yes. They can't find their own. And it also has been documented that when the vitamin D can't get to its own receptor, it can't down regulate itself. So, yes, not being able to regulate itself through its own receptor, it would rise unabated until the body stopped to express the vitamin D receptors. And it will reach a point where it does that. It's called VDR deactivation. And it'll cease to express vitamin D receptors. And at that point, the body's not going to release very much two 5d from the liver. There's not really any purpose for it to go and get activated because we're not expressing receptors for it.
Speaker B
Okay. And then on the subject of molecules going into other molecules, receptors, what about melatonin and vitamin D? Is it true that it can go in the vitamin D receptor in winter or whatever?
Speaker A
That I. The first time I heard that was yesterday. So I need to look at that and I. And I mentioned that I need to see which vitamin D receptor it went into. We've talked about the nuclear one today, you and I with the RXR. There's a membrane one and they are distinctly different proteins. And so I'm really curious about which one it went to. One's considered a rapid response receptor. It happens in seconds to minutes, whereas the pairing is a slow genomic response. So that's news to me. I haven't heard about that, stealing that. But I can tell you another swap out that we're seeing. And so normally the RXR is the pairing with the vitamin D receptor. Sometimes the p 53 protein, which is the guardian of the genome protein usually protects you. Sometimes it can displace the RXR. And there's a paper about that happening that I could send you.
Speaker B
I know that'd be really interesting because the other thing I wanted to ask about that this is, again, for more the public, because they have an obsession with snips and vitamin D SNP's. What's the story with that? Are those just snips that have adapted based on where that their ancestors sort of lived? Or does it matter if people have got snips or what's the story there?
Speaker A
There's a few snp's that I think matter. But they aren't going to be the VDR snips and the VDR one that's of concern. BSM. There might be one more letter in it, there might be four letters in it. But basically the BSM VDR one causes you to send the two five ds through to 125 D way too fast. Those people are going to have a lot of 125 D. So you definitely none of them really want to take it. But absolutely with that one that is seen. But when you read the literature on the SNP's, you see that they tell you the general population is low in vitamin D. Just because you have some vitamin D SNP's doesn't mean you need to be taking vitamin D. What influenced your genome there? Two things. The pool available genetics from your lineage, plus the photoperiod present at conception of your mother. That's what passed on your, what I call the MTHFR genome. And there's papers on that. It's meant to be an advantage. So if you're drastically different location now than where you were conceived, you might see something going on there that your body's probably going to adapt to. Epigenetics. Yeah, I don't think you're locked into anything like that. I think the body's way too versatile. I look at the body like a well designed machine that will work, run on any oil, run on any fuel, has multiple pathways to accomplish the same thing. This vitamin D, water soluble sulfate system, if you were going to sit down and design it, I think you would design it like it turns out to be. It just makes sense when you see how it works. So I just think that we have become convinced that our body doesn't have the capability to take care of itself.
Speaker B
Yeah, because I was going to say maybe there's all these snips, because isn't there like over 36 in this vitamin D system? Maybe the body doesn't need it or it doesn't want certain forms of vitamin D and that's it's deliberately like down regulating the production of it. And us stuffing more and more and more supplements in is sort of overloading a system because with the SNP's, like you, like you said, they're there to give an advantage, they're there for a reason, for that environment, because that's the other thing people get all panicked about is the SNP's. Oh, I can't make vitamin D. But as you were saying, it's like, well, which form can't you make? You know, because I think with the SNP's they're not particularly well understood. Or are they now? Or do they just focus on storage active and the receptor and they don't consider all these other intermediates.
Speaker A
I think everybody has their own different theory of how this stuff works. Like if you were to read Yasko's stuff on MTHFR or Ben Lynch's, they'd have different opinions of how to approach each SNP differently. There's a lot of time between the two of them studying that stuff, but still. Yeah, I just, I think it's a niche that people get into and try to figure out, but I don't know, I don't know. A lot of people making a lot of headway working on this.
Speaker B
Yeah, that's what I thought. Because just for the people listening, because I know the kind of questions I get asked all the time that, you know, not to get in a panic if it looks like you've got some interesting snips other than the one you mentioned, and not to get into a panic about the, the winter and your snips and suddenly start taking a ton of supplement. Right, yeah, because I want. Just on the subject of, just so we can wrap up, because you've obviously been very generous with information and time. We haven't talked about one thing, vitamin D from food and things like mushrooms, because they have a d two and then things like salmon and liver. And what happens when we eat vitamin D that got made by the sun because the animal was in the sun at some point. How is that different to the supplements?
Speaker A
You know, that's going to be your whole food stuff. There might be stuff there we haven't discovered. And I just. There doesn't seem to ever be a problem with that. In fact, there were some studies that looked specifically at vitamin D, vitamin K, maybe magnesium, and they said when they used it from supplements, not only did it not help, they saw some harm. I'll send you that paper, but they saw benefit from it being nutritional form. And I actually, I glad you brought that up. I did want to talk about the mushrooms in the d two world there today. Mushrooms are a world of d, depending upon the mushroom and their exposure. But what, what I find fascinating is, is we want to put them in the sun to have the ergosterol, if I'm saying it correctly, become the d two. Actually, any that doesn't get converted before you eat the mushroom, we have an enzyme that can do that. It doesn't have to be done with uv. It doesn't. It's not the same reaction. It doesn't necessarily make the same thing, but we have a way to assimilate that, too. But from what I've seen, the d two molecules are amazing. They are really amazing. There are active forms of them. I think that when people are on d two prescriptions, one of the reasons it doesn't increase their two 5d is because it doesn't go to a pathway that's going to make a two 5d form of it. It's going to make other, like a 20 form of it or a 17 form of it. So there are some pretty amazing d two molecules out there. So I definitely wouldn't hesitate to eat those. That's the only way you're going to get d two or d four is by ingesting it. You make d three. So just think about it, you know, just broaden your horizons there. It's going to make completely different things. And they're. They're anti cancer molecules and stuff. That's what I'm saying, is that they, they fight diseases and stuff.
Speaker C
Oh, yeah.
Speaker B
Because in Japan, they use medicinal mushrooms, like turkey tail, for cancer. And then the mushroom that grows somewhere is the amanita mascaria, the flyergaric, that's got something like a hundred times more vitamin D than others. But then, like you were saying, there's probably lots of forms. And then when we eat the salmon or the mushroom, it's going to be a big mixture of biological forms, not just one form, like the supplement. And then that's like you said. Well, like we talked earlier, a lot of the time with the food, vitamin a comes at the same time, and so does vitamin K and magnesium. So it's like other things are coming along when you take it naturally from the mushrooms or the. Or the fish or the liver. Have you got anything else to say about the mushroom? D two and d three molecules?
Speaker A
No, I would just say that they're very overlooked. And if you go and you target research on them, like the d four molecule or something like that, or do a d two pathway, just do an image of that and see what molecules are made. Once you start looking at those molecules, you're going to be asking yourself, why are we obsessed with two 5d? Why are we not talking about 1720 d two? I don't understand, you know, and so we're just focused on little tiny nothing of the world of vitamin D. Yeah.
Speaker B
So with the mushrooms, do they all make a lot of. In general, a lot, with a few exceptions, that make a huge amount. Are there certain mushrooms that are culinary that are better than others at making vitamin D or are they all.
Speaker A
Okay, you know, I. I don't know that any are better than the others. I have a few posts on my facebook about that and I put studies there with them and it named the particular mushrooms. So I will definitely get those for you. So you can put them out.
Speaker B
Oh, yeah, yeah. All people can look up because I think.
Speaker A
Right.
Speaker C
I think.
Speaker B
I think oyster mushroom or shiitake or maitake, but I don't know, I think it's obviously going to depend where it grew.
Speaker A
Right.
Speaker B
But just the take home message is look into the mushrooms. There's a lot more to them and they have their own special vitamin ds that are unique to them. And that could be because sometimes people say it's things like the beta glycans in the mushrooms that are doing the magic, but maybe it's not.
Speaker A
Right. It could mean a number of things. I always think of the miting your mitochondria, Ted talk by Terry walls where she says, eat this big old plate of vegetables and we know this in here is good for you. But what about all the stuff we haven't discovered yet? The stuff we haven't discovered may be way better than the stuff we have discovered, so you just never know. I do think that when I looked at the mushrooms and I looked at the enzyme that converts the ergosterol, I think that also continued on a pathway that made an anti cancer or some amazing molecule. So there's two different pathways. You let it become d d two before it enters you. You let some of it come in as a substrate of d two and you get two completely different pathways of d two established in your body.
Speaker B
Oh, yeah. That's fascinating, because just before we wrap up, because I was going to ask about mitochondria anyway, because there are BDR receptors in the mitochondria, aren't there? Because how does, what does, what's the relationship between vitamin D and mitochondria? How does it work? Why are the receptors in there?
Speaker A
I have never read a stitch of science on why they're there, what they do for it, to be honest with you, nothing. Which probably means that I should and it's probably super important.
Speaker B
Yeah. I don't know. What do you. Off the top of your head? Why? Because I have my theory of why it's in the. But what do you think it might be? Or do you. Because some people like to speculate. I do. Because, you know, whereas other people are like, if the science is not out there, I'll just wait for it. And other people have their own theories.
Speaker A
Right. You know, I would think probably its role inside the mitochondria would be back to its detox world, where it detoxes drugs and certain things like that. It's probably trying to keep a clean environment for the. For the. All the transfer of electrons and whatnot that needs to happen in there. Who knows? Maybe. Maybe it's playing with iron somehow. I, you know, I don't know. Trying to keep it a copper world. That's a really good question. I'm gonna have to look at that. I think it detox right off the top of my head. I'm thinking it might have to detox something out of there.
Speaker B
Okay, I know that's really interesting, because always ask, you know, it's nice to sort of have hypotheses, because then, you know, studies come from. From that. No, that was. That was really interesting. So, yeah, we've gone quite long. So thank you very much for your time. If people want to find you and follow you, where.
Speaker A
Where.
Speaker B
Where is it? Because you've got a really good substack, and you've got a Facebook group. Where can people find you? And have you got a book or a paper or. I know you just published a new paper.
Speaker A
I don't have a book. I just put out that paper on the water soluble sulfated forms of vitamin D on the substack that's under my name, Jim Stevenson Junior. If you just look Jim Stevenson Junior on YouTube, you'll find there's a lot of podcasts on there. And then my page on Facebook, Seiko steroid hormone D. That's just the real name of vitamin D. Those are the three places. And people can private message me if they want to. That's fine. You know, I like to talk to people. I like to see what's going on on, you know, it's important.
Speaker B
Okay, great. So thank you very much for your time. I really appreciate it, and I've been really looking forward to this for a long time. All right, thank you.
Speaker A
Thank you.
Speaker C
Thank you very much for watching. I hope you found this useful. So Jim has a sub stack all about vitamin D, so you can check him out there. Here's a spurty vitamin D lamp, and this is UVA and UVB, sort of pretty much full spectrum. And this is what it looks like turned on. This is a chroma D. So this has red light, near infrared light, narrow band UVB and violet light for opsins. And as you can see, it's smaller than the Sverdi, but then when it gets turned on.
Speaker B
So you can see.
Speaker C
It'S pretty powerful and you can burn yourself with this and asperti. And then here's a a. Here's the Krypton so you can see the size. And the Krypton has uva, uvb, red light and near infrared light. And it again is a narrow band UVB which favours vitamin D, making like the chroma. So if you're interested in these products, the links are in the description and use code doctorsera for a discount on the Krypton and the chroma D. I'll be putting a transcript and audio on Jim's interview in substack because there's quite a lot of material and some people might want to read. And I'll also put a bit more about the vitamin D making lamps. So thank you for supporting the channel.