Innate Wisdom Podcast

What It's About:

Today we’re talking all about Vitamin D with Jim Stephenson Jr. Jim is a Vitamin D researcher whose passion for research on the topic sparked because of a family member’s health issues, which included severe osteoporosis at the age of 51. She was prescribed 50,000 IU of vitamin D, which is a ton of Vitamin D, but this actually caused her vitamin D levels to decrease and her health continued to get worse. This incident gave him the incentive to start diving deep into Vitamin D research, applying his research and writing skills from his previous experience in the fisheries industry, and what he found was shocking. For the past two decades, Jim has been passionately researching and advocating on the topic of Vitamin D to help people learn and understand the other side.

Listen to hear more about:

- Myths and misperceptions about Vitamin D
- Is Vitamin D from the sun and supplements the same?
- Should you take Vitamin D if you’re sick?
- What is low Vitamin D? What does it really mean?
- Vitamin D & fertility treatments
- Vitamin D & sperm health
- Vitamin D & testosterone levels
- Do you need to take a Vitamin D supplement to support supraphysiological levels during pregnancy?
- Vitamin D & pregnancy complications
- Do you need to supplement Vitamin D while breastfeeding?
- Do you need to give your baby Vitamin D drops?

Transcript:

[00:00:00] Loren: Jim Stevenson, Jr. Welcome to the podcast. I'm so excited to have you. 

[00:00:05] Jim: Thanks for having me. I really appreciate it. 

[00:00:07] Loren: Awesome. So this has been a long awaited conversation, at least for me, but I know a lot of people will be really excited to hear from you. And today we're gonna be talking about a bunch of different things, a lot focused around vitamin D and, you know, some other things, but hopefully everyone learns something that they didn't know before about Vitamin D too and it helps connect some dots and fill in some gaps that they might have in their Vitamin D knowledge. So I like to start off by asking everyone kind of how they arrived in the place that they're at today.

So my first question for you is, can you tell everyone a little bit about yourself and what led you on the path you're on today and how you became such an expert on Vitamin D? 

[00:00:57] Jim: Sure. So, what ended up happening for me was I returned to school at a much later time in my life than most people are getting their degree.

And so I was engaged with learning already, and I've always been somewhat of a conspiracy theorist. I'll do research into certain things and stuff like that, and that was already part of my nature. But what ended up happening was a significant person in my life ended up being diagnosed with vitamin D deficiency.

And at the exact same time, anything that was wrong with her was also then lumped into that “this is all because of vitamin D deficiency” and things like chronic fatigue syndrome, fibromyalgia, osteoporosis, things like that, all lumped together, which are really common. A lot of women get multiple autoimmune labels, especially the ones I just said, add thyroid to that, adrenal fatigue, those kind of areas.

So what ended up happening was, there was a prescription written to take vitamin D, 50,000 IU once a week to get on track. This person's vitamin D was 23 at the very beginning of this. That was what they labeled. This is around 2009, 2010. This was just when the goal was really getting solidified, being changed up to 30, but it already on their radar even at 23.

And so taking the vitamin D prescription, the vitamin D level actually dropped to 11. The opposite of what you would expect. You would've expected the vitamin D to go up. And at that point it got my radar up and said, “How does that work?” This is a huge dose of Vitamin D 50,000 IU. How does vitamin D drop when you take that?

So stop taking the vitamin D. Started doing some research and I ran into Trevor Marshall's work and started reading about the active form of vitamin D because up until that point, the entire focus is on the serum 25 D hydroxy vitamin D. And at that point I didn't know that from the D three you took, I didn't know anything about vitamin D at that point.

So once I found there was an active form and saw that some people were saying “Not so fast. You need to measure the active form.” Some of the sick people will actually be high in that. And it took me a long time to find a doctor that would actually measure the active form. And so this person had been off vitamin D during all that time waiting only getting vitamin D from the sun and whatever's in the food that you eat, which you'll end up getting an RDA at least eating normal foods because they've put vitamin D in so many things.

But when we finally got that vitamin D active form result, it was 76 and the range is 18 to 72. So even avoiding the vitamin D and having a level of 25 D at 11, this person was still high in the active form of vitamin D. So that's how it all began. 

[00:04:00] Loren: Uh, the catalyst. That's so interesting. Thank you for sharing.

And the reason I love that question is because typically, everyone kind of has a personal connection to what's led them to become the expert or practitioner they are today. Whether it's their personal experience or somebody close to them, experienced an illness or something like that. So it's really inspiring and you kicked off that research, but hopefully it's been helpful to that person too. Are they okay now? 

[00:04:31] Jim: Yeah, we learned a lot along the way and that person is much better now. 

[00:04:35] Loren: That's great to hear. Awesome. So I would love to, because you kind of mentioned a couple terms already in introducing who you are and how you got here, but I'd love to first kind of dive into everything by you addressing some common Vitamin D myths and misperceptions so that we can expand upon a couple of terms and things like that and maybe a couple facts that people don't know so that it can set the precedent for all the other questions that are gonna come cuz it, you're gonna have to know a couple of terms or glossary terms, things like that.

So the first myth or misperception I'd like to address is the one that is the vitamin D you get from a supplement is just as good as the vitamin D that you get from the sun. Can we talk a little bit about why this is probably not correct? 

[00:05:35] Jim: Well, it's not correct for a couple reasons. Number one, scientifically that molecule is the same. So if you're talking about vitamin D three that your body makes from the sun or vitamin D three that they've managed to encapsulate in a pill, molecular wise, they are identical. But the fact that the pill has this isolated, concentrated amount of vitamin D that you know, really doesn't occur in nature like that.

So, concentrated without any other cofactors. And typically something we call a vitamin comes with all its necessary cofactors, and usually gets released through some sort of autoimmune-like reaction that releases the vitamin. They're the same in that sense, but the difference right away would be whether you're taking it or making it, even though they're in different places, they're the same molecule, they will be handled differently.

So when you go in the sun and your body makes vitamin D in the skin here, it's going to be picked up by the vitamin D binding protein that's its shuttle through your body starting from the time it's made, whereas the vitamin D pill goes into your gut and it's picked up by the lymphatic system first.

It's not like people think it gets picked up and it gets shuttled with LDL cholesterol and on its first journey. After that point when they both converge at the liver, then they both will be carried by the vitamin D binding protein on the rest of their journey to the kidneys and then to the tissues. But that first part is really important because even though there's the same molecules, they're shuttled differently.

And because they are shuttled differently, they impact your lipid panel too, because you have to have LDL cholesterol to shuttle the oral vitamin D your body picked up, and that's made with the same substrate that the vitamin D in the sun D three is made with. If you're taking vitamin D, you're using a molecule substrate called seven D hydro cholesterol to make that vitamin D in the sun.

But if you're not making your vitamin D, you're not using that LDL cholesterol, but you are then needing it to shuttle things around. It's just the inferior way to get vitamin D. That's why you only get a small amount at most, 10% of your vitamin D from orals, whether it be pills, whether it be food, salmon, eggs, things like that.

It's an inferior way of acquiring vitamin D three, to be honest with you. 

[00:08:06] Loren: Mm-hmm. Thanks for that explanation. And one thing also I'd love to touch on too is you mentioned the difference between taking it and making it isn't the kind that you make water soluble to, and that's important. 

[00:08:20] Jim: Yes, you make both kinds.

In the sun, you would make a fat soluble vitamin D three, and it's, I think it's typically called a conjugate. So you're gonna make a sulfated form of vitamin D three as well. Different enzymes do it, and that's pretty important, but there's not a whole lot written about that, unfortunately. 

[00:08:40] Loren: Mm-hmm. I hope we have some more research done on that too, someday.

And, one other thing too that I wanted to touch upon this myth is that when you make it versus take it, there's so many different metabolites of vitamin D, correct? And the sun, you kind of, it will allow the body to create those different metabolites, I guess, in a more supported and natural way, versus if you were just taking a D three supplement.

[00:09:13] Jim: That is correct, and some of those pathways aren't really open to the oral intake of vitamin D because when you're in the sun and you make the vitamin D three, continued sun progresses that molecule past what we know as D three into other molecules. And there's a bunch of them, and once it makes those, some of them can revert back, so they're like a pressure valve, some people refer to it as a pressure valve, so you don't end up with too much D three. But in reality, we don't study how much you need of those other molecules that it makes. We don't even ever really talk about that. So since they're made in the sun, you can rest assured your body uses them.

They're not all just waste. 

[00:09:57] Loren: Mm-hmm. Yeah. Thanks for that explanation. I like that analogy, the pressure valve. And even though there's not much research on those other metabolites, I'm sure that because they exist, they're probably pretty important. I think I've seen some of your shared research on, I wanna say 24 O- H-D three.

 

[00:10:20] Jim: Yes. 24. 24 is a molecule. In fact, I was just writing about a D two 24 D molecule a couple weeks ago. So you have your D three that becomes 25 O H D, D two or D three, either one. Depends on what the source it's made from, whether it's made from D two or D three. Once you have that molecule, there's just one set of numbers that means it's been hydroxylated, uh, hydroxy vitamin D, It's been hydroxylated one time. And so then when you move to the active form and there's a 1 comma 2-5 O-H 2 D three, it's been altered. Again, it has to do with the positions. Those numbers relate to a position on their carbon chain, and that's not really that important. So when you see a host of numbers like that, there's three levels, so there's ones that have three sets of numbers. 

That's just how many times the body's modified them to make all those different molecules. And every time it did that, it had to find the substrate, be it two five D or uh, 1 25 D. It had to find that. So it had to make it in the first place to then alter it and had to present the correct enzyme.

So there's all these decisions going on behind the scenes that you don't even know about. You can't just say, ‘Oh, I'm gonna take D three and I'm gonna get everything I need from it.” That can't happen. That's just not even possible. 

[00:11:46] Loren: Mm-hmm. Thanks for elaborating on that. That's very helpful. And or , maybe it's making more people confused, but we'll see.

Hopefully you guys are following along. Okay, so the next myth or misperception I'd love to address is, you’re low in vitamin D if your levels are lower than 25 nanograms per milliliter. You kind of addressed this a little bit already, but there's also a borderline range now, which is 25 to 35 nanograms per milliliter, so I'd love for you to touch upon that, especially because you have personal experience with somebody in your life taking tons of vitamin D and actually lowering their vitamin D status.

[00:12:32] Jim: Right. So what ended up happening was there used to be a much lower goal, 12 and a half was the goal before, and they asked the Institutes of Medicine in New York Academy of Sciences, “they” being Canada and the United States, asked the IOM to please evaluate all the existing literature on vitamin D and look at adjusting the recommended daily allowance and the goal.

And they were really most concerned with the recommended daily allowance. Okay. And then they would look at what that would get from the studies. And so they looked at all the studies and they decided that a level of 20 would be fine to cover almost the entire population, but they immediately were scrutinized over that because there were a lot of other people who thought we should have much higher levels of vitamin D and some of them had a lot of influence like Michael Hollick and through the influence with the Endocrine Society and, and the way they cite one another's papers, they were able to get most people to move to a 30 plus goal for the 2 5 D.

And so in around 2010, overnight, millions and millions of people were declared deficient the very next day because the goal had been raised. So that in and of itself can be an issue because when somebody has a vitamin D deficiency, it needs to be in the active form, first of all, because that's what the body's going to use.

But you have to have some clinical signs of a deficiency. And instead, what we have is we have them taking everyone's two five D from everyone that's willing to have a lab regardless of their condition. And they've worked it now where they're actually blaming almost all human disease on the 25 D level in the people without ever looking at the active form.

So most of the things that we see on a symptom list, Can't even be attributed to the active form of Vitamin D. One that I see all the time is sweating from the forehead is supposed to be a symptom of vitamin D deficiency. Then that's only because so many people have vitamin D deficiency and most of them also sweat from the head.

So they become, uh, correlation equals causation. And that's what has happened all built around the 25 D molecule. And most of that is possible because they raised the goal. If they hadn't raised the goal and people weren't getting labeled deficient in it, you wouldn't be able then make the Segway to blame some condition they have on it.

First you had to make sure that everybody was deficient and that's what the new goal accomplished. 

[00:15:19] Loren: Mm-hmm. Okay, so we have a couple things going on here. So the first one is that the goals have been changed pretty significantly. More than doubled, I think, right? 

[00:15:31] Jim: Yes. More than almost tripled. 

[00:15:33] Loren: Almost tripled when there may not have been any sort of, rationale, or I would say supported rationale for it.

And actually, I would like to point out, if you wanna read more on this, there's a really interesting, actually, coming from the New York Times, there's an article about Dr. Michael Hollick that is sponsored by certain labs. I will put that link to the article in the show notes. You might wanna read it, and that can kind of elaborate on, I guess, a timeline of when these changes occurred and maybe the impetus for that.

So, we have the ranges changing. Maybe without substantiation. And then we also have the fact that we might be looking in the wrong place to assess vitamin D status. So you mentioned we have storage D, so 25 O H D three, that is the inactive form. And we have 1 25 O H D three, which is the active form. And you're saying that the active form is what we should really be looking at, but, what doctors measure, and especially regarding your personal experience with it, the storage form was being measured and that's what had the doctor prescribe 50,000 IU of vitamin D for your special someone. So. Right. Yeah. Okay. Just wanted to get that straight. And I think there's also another aspect to this too, where blood may not be the best form or method of assessing status of D anyway because it is a highway for hormones. Can you talk a little bit about that?

[00:17:21] Jim: Yeah. The problem with trying to use it as the marker is that a lot of people assume that if that's low, like let's say it's at 15, that that means that there's not enough vitamin D two five D substrate to make ample amounts of the active form that you need.

But what we find out is that the sick people. They actually already have high levels of the active form. The active form is the molecule of immune response. So if you have Lyme disease or any kind of viral thing going on at the time, that's the molecule the body makes because that molecule is able to, through your DNA, make things that fight for you.

It makes what I call chemical and biological warriors, and that's the form that does it. Two five D doesn't make anything except turn into the 1 25 D and then using some vitamin A and the vitamin A receptor, they together make things like macrophages, T cells, antimicrobial peptides. The entire reason a person wants vitamin D for their immune system is through that molecule, so it doesn't work out that you don't really run out of 25 D in your blood, like people seem to think. 

In the winter, for example, you can look at healthy liberation of vitamin D in people. They can liberate between 3,000 and 5,000 IU of D three every day from storage. They're D regardless. I don't remember which metabolite they were looking at, but every day these people, that's a lot of vitamin D to be releasing in the winter and it'll definitely help you through the winter and that's why it's an absolute farce, a lie, I would say that we have a vitamin D deficiency come winter. Just because we're not making D three, we're not making two five D out of that D three directly like we are in the summer. So two five D, depending upon what lab, what time of year and what else you're doing, it will drop a little bit.

But that's natural because that's where the D three is coming through to. That's when you're gonna liberate that in the winter. There isn't a seasonal variation in the active form. There is a seasonal variation in the storage form, but they aren't connected like people think you can have a very low 25 D with a super high 1 25 D, like I said, for the significant other that I had.

[00:19:58] Loren: Mm-hmm. Great. That's really helpful. So one thing I wanted to point out is that you can have a seasonal variation and it's kind of unavoidable with the storage form, which is what we typically see and what doctors are like, “Hey, it's winter and your vitamin D's below, or it's low”, but there's no technically seasonal variation with the active form, which is what we want and need anyway. Correct.

Okay. Just wanted to clarify that, and I think this is a good segue into the next sort of misperception too, which is you should take vitamin D if you're sick. So I think you kind of alluded to that already in terms of sick versus healthy, that there's typically a lower level of storage D and the differences. Sick people have a higher active D, but can you elaborate that on a little bit? 

[00:20:51] Jim: Sure. So certain things I talked about a little while ago, certain viruses, let's take Epstein-Barr viruses, a really good example. A lot of people have Epstein-Barr virus flaring. They don't just have it and back in high school and have mono, the kissing disease for a little while and get over it.

Some people have problems with the Epstein-Barr throughout their life and when it's replicating, its presence in your body will be causing two five D to be activated into 1 2 5 D. Okay? So its presence in your body causes the immune response molecule to be made so that it can make things to fight Epstein-Barr like macrophages and T cells and antimicrobial peptides.

But the reason Epstein-Barr is still around and flourishing is because it's evolved to block the action of vitamin D. So when you have an antigen test for Epstein-Barr, some of the antigens that they may be looking for, E B N A 1, 2, 3. These three antigens have the ability to park in the vitamin D receptor, so they're in your body.

They're causing your body to make the active form of vitamin D to respond and fight them. But once that form of vitamin D is made, it can't get to its receptors. So it can't do its job, and what ends up happening at that point is it can't down-regulate itself. So it starts to get high, and that's what you see in sick people.

Then the body, through the control, which is the BDR, the vitamin D receptor gene, it realizes that it's unable to down-regulate itself. So it stops expressing vitamin D receptors in your body. Which sets your sensitivity and that causes you to stop absorbing as much vitamin D through oral routes and making as much through skin routes and things like that because it's going to protect you from excess vitamin D that doesn't have access to the receptors.

And one of the reasons why is because once it's not tightly regulated, it will go and steal other nuclear receptors. There's a host of nuclear receptors in your body. Vitamin D receptor is a nuclear receptor. All that means is that when it's doing its real work, it goes into the nucleus of the cell. That's why it's called a nuclear receptor.

But other nuclear receptor systems like the thyroid and adrenal and glucocorticoid can be stolen by 1 25 D that doesn't have access to its own receptors anymore. So that's why the body will down-regulate 25 D in a sick person and have high 1 2 5 D at the same time. That's the body's reaction to certain pathogens that are able to block the vitamin D system.

[00:23:50] Loren: Wow. That is fascinating and that's definitely something that I wanted to touch later on so I'm glad we're covering it now. So we have a couple things going on here. The body will up-regulate active D to support an immune response. Correct. But certain viruses can block the receptors, which causes the active D to stay high.

So when the body senses that, it will downregulate the production of D three to protect the body from hypervitaminosis D, so over time so that the conversion from storage D to active D is slowed down because for the active D, there's no receptors or at least less receptors. And that can be problematic too, if there is too much excess active D and not enough receptors because the active D will look for other receptors for other, I guess, functions in the body that will suppress the other functions from working properly. Like thyroid and progesterone, like you mentioned. 

[00:25:02] Jim: Right. Yeah, it would regulate how much D three it's making in the sun and other things.

But another main way is the BDR, the vitamin D receptor gene stops the expression of vitamin D receptors as well, and so a lot of the oral would just pass on through. It's not a very efficient system to begin with. It just ignores more of it because there's no receptor to make to pick it up. 

[00:25:27] Loren: That is so interesting. The body is amazing and very sophisticated. 

[00:25:32] Jim: It is very, It's very smart. 

[00:25:35] Loren: Yes it is. So what do you think about the 10,000 IU per day that a lot of people are getting prescribed right now? That was kind of like the standard daily dose of vitamin D. 

[00:25:48] Jim: The thing is, that's so much vitamin D. Hector DeLuca, the grandfather of Vitamin D, as I referred to him, he said, You should never really take more than 2000 IU of vitamin D at a time, because there's not a whole lot of safety data on that. And even to this day, there isn't that much safety data on those kind of doses because we don't track where they go or what they become. So none of the science talks about utilization. 

No one has any formula where they say 10,000 IU of D three goes in, this percent makes it and progresses to D three, and this much progresses to 1 2 5 D. And once it does, it did these biological acts. No one's tracking if it even stays in the people to begin with. And the only way we can track to see if it's in people is with a serum test, a blood test.

Whereas most people, Would store oral vitamin D in some fat, or it'd stay in the liver or it'd go into your muscles. So most of it, we can't even see where it's at. In old papers, you can find old papers where they would radio label the vitamin D to see where it goes and what it did and what it became.

But in spite of all our modern technology, the science is kind of stone age now compared to the seventies and eighties, unfortunately. 

[00:27:17] Loren: Mm-hmm. Yeah. That's interesting. Yeah. A lot of people are taking that every day to avoid what's going around right now, but it is quite a bit, especially if you're hip to what we've been talking about already.

And I also wanna point out to something that you mentioned earlier, is that we also need vitamin A retinol to activate that vitamin D. So there's a lot more sophistication around this than we realize, and I guess that's also why Vitamin A is called, Well, it's the original antiviral vitamin, isn't it?

[00:27:52] Jim: That sounds right. Yeah. 

[00:27:54] Loren: I think earlier last century, Vitamin A was a remedy for viruses and things like that, and that's why people were being given cod liver oil, which also has Vitamin D in it. Nature's so smart. It pairs the two together. Right. And we also need nutrients like magnesium and zinc and sulfur too.

So there's a lot more than just D that we need for it to function properly too. Right. So now that we've gotten a few foundational concepts out of the way, I would love to talk a little bit about vitamin D in fertility. So there's some research that correlates higher vitamin D levels with higher rates of fertility in fertility treatments, or success, I should say, in fertility treatments.

And then there are those that say it makes no difference. What would you say is right about this, or what's your take on it?

[00:28:52] Jim: So the problem with, the bad part of vitamin D where they're talking about a deficiency as well as the good part where they're saying vitamin D seemed to help or make a difference over here in this group, is all built around the fact that they started with two five D.

So everything telling you Vitamin D deficiency is causing a bad outcome, be it cancer or fertility issues, or the current pandemic that we're living through right now. Any of those things, they're all built around what the person's two five D level is to begin with without ever looking and seeing what they're active form is.

So first of all, The only way that somebody's deficiency in two five D can be the cause of their cancer per se, would be if they were also low in the product it becomes 1 25 D. Any associations that are drawn on 25 D with disease go away if they weren't also deficient in the active form. So it's a house of cards, and so you don't see anybody measuring the active form to confirm that they were truly deficient because you did not deficient in the example that I began with the person I'm talking about that had 11 as their two five D, but had 76 as their 1 2 5 D. That is not a deficiency. You cannot start blaming the 11 2 5 D with their illness. You could blame hypervitaminosis D probably at that point with some of the things that are wrong.

So they start off, first of all, with a correlation and they turn it into causation. So they're telling you that two five D is a cause of almost all human illness today. That is actually ludicrous because it can't be the cause of illness. It doesn't do anything but become other molecules that do something.

So let's talk about when they take a bunch of pregnant women and they measure their two five D, and they're going to then associate the two five D with. Okay, they're gonna say the people that had higher, more replete two five D did better in certain things like preeclampsia and, and all those other things.

But keep in mind, this wasn't a group that they are intervening with. Most of them, it's what you show up with is your vitamin D level, your two five D level. And there's a lot of non-treatment where they're just looking at the data. And in those studies, they can blame without measuring the active form two five D with all those negative outcomes because the sick people will have lower two five D as we just discussed, the reasons why.

If you have layers of Epstein-Barr virus and your body already has high 1 25 D and is protecting you with two 50 D, now you're pregnant. Anything that goes on with you is gonna be blamed on that low two five D, even though we just explained the mechanism by which it became low. So they're blaming the wrong molecule and it's the opposite of a deficiency.

Most of those people have hyper vitaminosis D. 

[00:32:11] Loren: Okay, so couple things here. There's not really causation associated with these studies. First of all, it's correlation, which doesn't mean that the deficiencies is actually causing these problems. Then we have, again, I like to think of it as more of a symptom of low D being, I guess, blamed as the cause of the issues.

So, low vitamin D, storage D, What Jim is trying to say, I think, and correct me if I'm wrong, is it's a symptom of a bigger issue or high active D, whether that be because of a virus or you know, the mechanism we just talked about, not necessarily the cause of these problems. 

[00:33:02] Jim: The literature likes to refer to it as a marker for illness rather than the cause.

Low two five D is a marker for illness. So let's say we're gonna have an interventions with this current pandemic we have, and we're gonna bring everyone in that tests positive for the C. And so they're gonna bring them in and first off, from what we just talked about, the people with lower 25 D are gonna be the ones that have diabetes, cancer, tuberculosis, Epstein-Barr issues.

So they're already gonna have lower 25 D cuz they already have a comorbid condition. So they're gonna have lower 25 D because the body may be downregulating it already. Mm-hmm. And what's gonna happen is then they're gonna take all those people and they're gonna say, we're gonna give them vitamin D.

So they're gonna give 'em vitamin D, and what they're gonna look at is they're not gonna pay any attention to how much vitamin D some people take without a rise in their two five D. All they're gonna then focus on is who's able to increase their 25 D, and they'll just throw however much vitamin D is necessary at it.

And so then after you've intervened, you're gonna have the people who were unable to raise their two five D and it was low to begin with. and you're gonna have those that were able to raise their two five D. The ones that were able to raise their two five D didn't have the comorbid conditions. They came in with higher two five D.

They were able to raise it and they did better because they don't have low two five D as a marker for any illness, cuz they're the healthier people to begin with. Mm-hmm. Does that makes sense? Yes. So it's a self-fulfilling prophecy. That's how they do it. And they'll give them the vitamin D and they'll say, “Look, the ones who increased.”

But they'll never have an explanation for, “how did some of these people take tens of thousands of IU and their vitamin D didn't go up? Where is it going?” You don't use it up getting and staying sick. That doesn't make any sense, but that's what it looks like. 

[00:35:10] Loren: Yeah. Again, it's the symptom, not the cause is really what I see.

Right. So I do wanna mention to you, just on the topic of fertility itself, I did find some interesting research that says 1 25 D is associated with a good estrogen and progesterone production, which is important for fertility, but there's also other research too that says that too much vitamin D, and so this vitamin D that they were measuring is 25 OH D, so the storage form, but even that too much D can be a problem for corpus luteum function and can also significantly decrease rates in IVF too.

So even too much storage might not be super great anyway. 

[00:36:03] Jim: Right. 

[00:36:03] Loren: So just very interestingly enough, I found some of that stuff. So I'd love to also talk about sperm motility or you know, male fertility. I do get a lot of questions from males just working on their fertility, trying to get pregnant, or also just trying to increase their testosterone, and they're all gung ho about vitamin D supplementation because they strongly believe that it increases testosterone.

So, I'd love to hear your thoughts or any knowledge that you have to share on vitamin D in its relation to sperm parameters and testosterone levels. 

[00:36:48] Jim: I looked at some of those studies you had there and what I noticed is the first two I looked at, they were doing the same thing where it was how the people came into the study, what their two five D was, and there wasn't an intervention type study and they were just drawing conclusions based upon their two five D level and the more positive things they saw as it was higher. 

Mm-hmm. And again, we're talking about the healthier people to begin with, so I would expect their sperm motility and all those sperm related numbers to be better. Just because they're naturally have a higher two five D, they don't have a comorbid condition, they don't have anything driving it down. 

When you look at other vitamin D molecules without getting too complex, other pathways, we don't talk about of vitamin D, they are intricately involved in all of the steroidogenesis from pregnenolone on right at the very beginning of this molecule. So they aren't the molecules that are in the pathways that we're talking about today, the D 3 2, 5 D and two five D. 

But vitamin D has a very, very strong influence in other steroids, which would include testosterone of course, but nobody is tracking the molecules in those more steroid like pathways to really tell us what benefit, what molecule is beneficial to helping the fertility in the sperm.

That's what gets lost along the way when you just want to focus on this one thing, 25 D. Without seeing what it becomes, how are you ever gonna bring those other people up to speed that didn't do better in the trial, didn't raise their two five D if you're not looking at the mechanisms by which you think they can get better? You just take more vitamin D three as the answer supposedly to everything.

You see that in the deficiency groups, you have one person doesn't have to take any vitamin D to have a healthy two five D, and you have other people that were taking 20 and 50,000 and their numbers are either staying the same or dropping. Why don't we look and see what's happening? If you were trying to feed a starving person with protein, there'd be some other lab workups.

They'd wanna see where it's going, what it's doing, what it's becoming, is it staying in the body? But we don't get any of that for vitamin D. 

[00:39:08] Loren: That's a great point. Yeah. So again, here we have. A lot of correlation but not causation, and there's a lack of tracking the exact kind of metabolites or molecules I should say, that are actually supporting testosterone production.

That's not to say vitamin D isn't important for fertility, but if we are going to hang our hat on supplementation, then we probably wanna understand a little bit more what's happening. 

[00:39:39] Jim: Right. One of those papers that I was looking at, one of the pregnancy papers, it had, they replete people did better as far as reproduction, but they never actually checked anybody's 1 25 D.

But I did find a paper inside of one of them. There was a citation, citation 29 in one of those papers. And I looked at it and I went to it and it was a mouse study, but they injected 1 25 D into them. So you have a paper that's not measuring any 1 25 D citing work that is only 1 25 D. And it's not in humans either, but it's there to support a human pregnancy study.

So you have to really, really look at what they cite and how they cite it, and when it really gets important. They will always be pointing at 1 25 D because that's where all the biological connections are, but it's usually only in the citations. I looked at every one of those papers and I searched them for 1 25 D, and only one of them had that in it, and it was a citation. Wasn't something they were actually talking about.

 

[00:40:49] Loren: Yeah, and even when you go to the doctor, if you ask for 1 25 D, they don't know what you're talking about. So I think there could be probably a lot of confusion. Again, it's selectively choosing things to support the argument without actually looking at critically the information. I do wanna also to reinforce what we just talked about, fertility too, again, Vitamin D is important, but like Jim said, that the level of storage, D, if it is higher, likely there's less illness going on, which by default your storage D is going to be higher anyway. 

So just looking at the sort of health of the people that are likely being researched upon if somebody has low vitamin D to begin with, they likely have something going on where supplementation may not be the answer or achieve the result, as well as with somebody healthier that can actually utilize the D better because their mechanisms aren't being suppressed because of whatever's going on.

[00:42:01] Jim: Right. 

[00:42:03] Loren: Okay. So hopefully you guys are all hanging in there. I know this is a heady conversation, so I would love to jump now to pregnancy cuz this is a really hot topic. So if you've been following what I'm about to say, hopefully you understand, but, For pregnant women, it's pretty normal to have active Vitamin D levels.

Correct? Because from what I understand, it rises to supra physiological levels, so exponentially higher, which makes a lot of sense because there's a lot going on while you're pregnant. You have a fetus that's growing, so your immune system needs support, but also it needs suppression. You have placental function happening, which also requires vitamin D.

You have hormone levels fluctuating, and a lot of steroidogenesis, so a lot of creation of new hormones. You also have calcium absorption increasing by a hundred percent, which Vitamin D supports. So I would love to hear your take on the supra physiological levels here. 

[00:43:10] Jim: Well, I think one of the key things there is the calcium.

So you have this situation for eons where women have been encouraged to make sure they get ample calcium because if they don't, it's gonna get stripped from their body and they're gonna pay for it afterwards, either through bone loss or that's why they take those big old pills of calcium, whereas, Like you said, vitamin D is involved in that and what people need to realize is that it's the active form of Vitamin D that's involved in that, not the 25 D.

And you notice the vast majority of pregnant women will get labeled deficient in 25 D. But they will have very high of 40% spikes in 1 25 D since that's the one that's involved in the calcium axis, the hypercalcemia control axis. It makes sense that that spikes on its own. Women didn't have to take a bunch of D three to make two five D to get the 1 25 D to spike like that.

The body knows to do that and does that, and it's not at the expense of losing vitamin D like it is with calcium because your body has a lot of stored vitamin D and it doesn't need that much of it really, to be honest with you. Mm-hmm. So that's really important to pay attention to, is that they already have a really high level of 1 25 D, so they are not deficient in any way, shape, or form.

But to further complicate things is that there are other molecules, and this goes to what we were talking about a minute ago, just because sick people have lower two five D and some of them were given vitamin D three to like if we are in a C epidemic trial group right here and we're giving them, they might not be raising their two five D because those inputs are becoming other molecules, and that's huge when it comes to pregnancy because babies and fetuses use other forms of vitamin D. 

Just because we don't talk about those other forms of vitamin D doesn't mean that their body doesn't need it. Children make a ton of vitamin D in the epimerization pathway, whereas a pathway we're talking about right now is the hydroxy pathway. Hydroxylation.

So just because your two 5 D isn't all that they think it should be, you need to look at the active form and you need to consider other molecules. Adults don't have very many epimerization form of molecules, but they do, if they have illness, if they have diabetes and other things going on, they will have a lot of those other molecules.

So you just have to keep in mind that there's a lot of molecules and you can't force the body in which one to make. You see that in pregnant women, their bodies are choosing to make a lot of 1 25 D guaranteed it's tied to the calcium needs for the fetus. 

[00:46:01] Loren: Yeah. Wow. There's a lot going on there. That's so interesting though.

I would love to follow up that question with another one related. So a lot of experts say that it's important to take vitamin D supplements during pregnancy. Specifically aound 4,000 IU to support super physiologic levels. So they're saying by taking a lot of D three, you're gonna support the storage form, which will then support the super physiologic form.

So they're really hanging their hat on that. And then there's also other rationale. Because that specific dosage also is associated with no poor outcomes or ill effects. Low levels of storage D are associated with gestational diabetes, preeclampsia, preterm labor. I mean, I could guess what you're gonna say there.

And that supplementation may help reduce these issues, although it's never necessarily been proven. And then we have a level of 40 nanograms per milliliter, so higher than that 30 current standard of replete sufficient D status to 40 nanograms per milliliter being maximal for reduction of preterm birth rates.

So I know that was a really long question, so let me know if I can repeat any piece of it. But the first part, what do you think about experts recommending uh, D three supplements to support that super physiologic level that our body's getting to for active D during pregnancy?

[00:47:42] Jim: Well, I can see why they believe that number being beneficial, and it's back to the associations and the correlations equals causation.

So when they're only measuring the 25 D, they found that those women that had 40 or higher in their blood did better, but they never looked at their active form, which I know you knew I was gonna bring up. And so the real science that's to be had in this study would be to take those people and measure both forms because if somebody that has higher two five D also has lower 1 2 5 D than the people with poorer outcomes, that tells you that more vitamin D isn't the solution because the sickest people have the highest active form of vitamin D.

It's wrong to think that sick people have low vitamin D. It's the marker we're looking at. I can assure you that they actually don't have low vitamin D. Most of them have normal 1 25 D, and a lot of them have high 1 25 D.

Like the example we started with 11 and 76, that's quite common. I recently took the numbers from 25 members of my vitamin D page. And they gave me two five D and 1 2 5 D, although 88% of them were low in 25 D, zero of them were low in 1 25 D. In fact, four of them were high in it, so it's the marker they're looking at.

That's why it's a self-fulfilling prophecy. Is because you're stopping and looking at the substrate rather than looking at what it's gonna become. So if we wanted to find out what is the healthy level of 1 25 D for the women, we're never gonna get there because they won't even measure it. 

[00:49:35] Loren: Yeah. So we have incomplete truth here, and it could make sense that the higher the storage D during pregnancy could be associated with better pregnancy outcomes because again, the comorbidity piece that we discussed earlier, right? Likely by default they're unhealthier. Something was going on maybe preconception or during pregnancy that is causing that active D to, again, maybe increase so much that the body is sort of suppressing or regulating that production there and down regulating the production of storage D.

Um, so I have seen, I couldn't find the study to send it to you, but I think it's one that you might be familiar with. There is one interesting study that has storage, active parathyroid hormone, and one other marker, and it measures Vitamin D intake at different levels. I believe maybe this is breastfeeding though.

[00:50:45] Jim: Yeah, I think I know which study you're talking about. It's the study that they gave 6,400 IU to the one set. If it's the one I'm thinking about, everyone's vitamin D went up at the different dosage. I think there were two dosages is the one I'm thinking of two.

[00:51:02] Loren: Maybe it was two and zero, like nothing. As one of the variables, or maybe that was a control, and then they had two different variables for the dosages, or it could be three different dosages and the control was nothing. I can't remember, but I have it pictured in my mind. I just can't recall exactly which one it was.

[00:51:26] Jim: I think I know which one you're talking about. I think it's one that I've talked about in other ones. There's four graphs. There's one of PTH, there's one of D3. There's one of two five D and one of 1 2 5 D, and all the women were at one of three doses, I believe. I believe that's that study, and we didn't talk about this earlier, but I'll throw this out there real quick.

By raising the goal to 30 plus, it's caused people to take enough vitamin D that they now store D three in their body, which isn't normal. Normally you wouldn't get so much D three that you would store it, but the magic number at which that switch happens is around 80 nano. And I don't know what that is in the NG right off the top of my head.

I know 60 is 24, for example. So it's normal. It's a normal level. It's probably around 40 I'm guessing. But once you get that much two five D in your body, 80 nanomol. That's when you start to increase the amount of D three in your blood, and that's shown pretty well on that graph that you're talking about.

And I'll send those graphs to you and then you can put 'em at the bottom of this. And it is a pregnancy study? Absolutely. 

[00:52:42] Loren: Okay. Yes. So can we repeat what the outcome of that was? Because I thought it was really interesting and I remember looking at the graphs, and I think we discussed it too, where the higher the input of D didn't necessarily raise anything to a significant level.

[00:53:02] Jim: That's right. There's two different studies. I'm thinking of one I mentioned earlier, plus this one in the pregnancy one. This pregnancy one that I just described with the four graphs, that's the one where everyone lost bone. Even 400 IU people lost 1.2%. I think bone. And so that was a study about unexpected outcome from vitamin D supplements, bone loss.

The other one, the other is a breastfeeding study, and they wanted to increase the breast milk content of vitamin D, and they used 400 IU and 6,400 IU. And when they were done, the levels at those two different doses, keep in mind one of those doses is a factor of 16 higher than the other. The end result of the children, I'm going off my memory, the end result of the children, they had moved their vitamin D from the teens, both groups, fourth hundred IU, and 6,400 IU into the forties. The difference was that the ones getting 400 IU were at 43 and the ones getting 6,400 were only at 48. Only five points higher for 16 times the dosage. 

[00:54:18] Loren: That's right too.

I remember that one as well. And that was gonna be my next question because their post-pregnancy, there's tons of pressure from midwives and doctors to take vitamin D supplements, and there's very limited, if not no vitamin D in breast milk. And because of that, people think, “Okay, if there's no vitamin D breast milk, we have to supplement because it's a really important nutrient where God didn't put vitamin D in breast milk for a reason, probably, or at least…” 

[00:54:51] Jim: I'm gonna agree.

[00:54:52] Loren: I think he wouldn't have forgotten that. So I think the standard dosage is around 6,000 to 6,400, which is what you just mentioned. So from this dosage, what we're seeing is even an excessive, so 6,400 compared to 400, which is in one serving of cod liver oil. It's like the daily value or daily allowance produces very similar results, right in vitamin D in baby.

[00:55:20] Jim: Right. It's even enough to cause bone loss in those pregnant women, 400 IU. And when we're talking about 400 IU of oral vitamin D, this is where people will jump on their cofactor bandwagon. They'll start to want to talk about vitamin K here, and that's a different thing. You can't avoid 400 IU orally eating like a normal person.

Going out and eating without a special diet, you're gonna end up with 400 IU. So you can't blame that on them not taking vitamin K or these other things because it's such a tiny amount. Nobody expects they're gonna have to gear up just the 400 IU. With cofactors, it just shows that we don't need that excess pill of isolated vitamin D. Even at that level.

[00:56:11] Loren: Yeah. That's so interesting. Hopefully that helps clear some stuff up for, especially for the breastfeeding moms. So in addition to mom taking vitamin D supplements for breast milk, we also have the pediatrician saying, “Hey, take vitamin D drops, put them on your baby's gums.” And typically the dose is around 400 IU.

So I would love to know also, what your take is on this too. 

[00:56:40] Jim: So there are some papers and I'll need to give them to you so you can share them. When mom supplements, carrying the child, or when we start to supplement the child right after birth, these pills, these supplements end up mostly making it into the epimerization form of vitamin D.

And I have very specific papers that talk about that. Adults don't have very many of the epi form of vitamin D unless they have some illness. And so what can end up happening? Let's say you give baby, maybe you're having your baby tested right away. Some people are obviously, so you're giving your baby these 400 IU drops and the baby's getting a two five D lab and the baby is labeled to have a level of, let's say 20.

And they are gonna want you to increase that dosage for the baby. And when we measure two five D, we're really only measuring a couple of the two five D molecules that exist. We aren't typically measuring the epi form of two five D or another 12 or so other forms of two five D, and the reason a baby might be making the majority of their two five D in the epi form is because number one, they're supplemented. Number two, it doesn't affect calcium. Maybe their body has a need for some vitamin D, but it doesn't need the calcium influencing molecules, and that's what two five D and 1 25 D are. That's the calcium side of the metabolism. It's very dangerous to play there, so the child may have 60% of their vitamin two five D might be in the epi form. So your test is only picking up 40% and you're gonna continue to give 'em vitamin D. They're going to continue to make 60% of it in the epi form. They're gonna stay labeled deficient throughout that whole process. 

[00:58:33] Loren: That's fascinating. So they use a completely different pathway, younger children, babies, and testing their D with the current way that we test.

So D three via 25 OHD, which is storage, is not necessarily an accurate reflection of their D status because it's something completely different.

[00:58:52] Jim: Yep. It's just one subset of the 25 D molecules. There's a ton of different ones, and each one serves a different purpose. There I found three pathways. There's hydroxylation we talk about, that's the one everybody's focused on, the two five D, there's the epimerization that I'm talking about. Now, your body also has another pathway called Lactones, lactonization. So those are a whole nother set of molecules. And so you start to realize that we're really only talking about this little, tiny, tiny bit of the whole vitamin D world. And so once you find flaws in testing on top of that other major flaw, you just start to see the magnitude of error in buying into the everyone's deficient story.

If you get your two five D to this right level, you're gonna miraculously avoid almost every human illness because we're blaming everyone on it.