How to Determine What Your Optimum Level of Vitamin D Is With Dr. Chris Masterjohn, Ph.D.

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What is the best level of vitamin D? This can be a tough question to answer because there seems to be conflicting opinions and research. Today we speak with Dr. Chris Masterjohn, who provides a radically different but highly logical approach for determining what your personalized and ideal levels of vitamin D should be.

If you need help determining your ideal level of vitamin D, click here.



Episode Intro….. 0:58
Chris Masterjohn Ph.D. Bio….. 1:47
Big Picture on Vitamin D….. 3:08
Vitamin D as a Marker of Ill Health….. 9:56
Low 25-OH Vitamin D Levels and Parathyroid Hormone….. 12:38
Vitamin D Polymorphisms….. 30:22
Vitamin D and Sex Hormones….. 38:22
Episode Wrap-up….. 1:03:33


  • Dr. Ruscio’s Recommended Vitamin D/K Supplement
  • Vitamin D treats thyroid autoimmunity
  • Vitamin D Treats IBS
  • Previous Podcast on Vitamin D
  • Chris Masterjohn’s Website
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    How to Determine What Your Optimum Level of Vitamin D Is With Dr. Chris Masterjohn, Ph.D.

    Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. I am here with Chris Masterjohn to talk about vitamin D. Super happy to pick this bright young man’s mind on the topic. Chris, thanks for taking some time to be on the show.

    Dr. Chris Masterjohn: Thank you so much for having me. It’s good to be here.

    Episode Intro

    DrMR: I’ve heard you speak quite a bit on vitamin D. We run in some of the same circles, of course, at the Ancestral Health Symposium, at Paleo f(x). And you’ve definitely been someone on my list for awhile whom I would love to have an expanded narrative on vitamin D because I do think—and from what I’ve seen from your writings and recordings—I think you’re at least partially in agreement with the health benefits of vitamin D may have been a little bit over exaggerated. And the levels people had been or have been shooting for may be a little bit excessive. And I think where we see eye to eye is maybe a little bit more of a reasonable position on vitamin D.

    Chris Masterjohn Ph.D. Bio

    DrMR: But I guess before we even jump into the topic, in case anyone hasn’t heard of you before, can you tell people a little bit about your background?

    DrCM: Sure. I have a Ph.D. in nutritional sciences from the University of Connecticut. I finished my Ph.D. in 2012. I did my post doc at University of Illinois at Urbana/Champagne for about two years after that. And I’m currently assistant professor of health and nutrition sciences at Brooklyn College in Brooklyn, New York.

    I have been active on the internet since even before that. I first started writing about nutrition in 2004 when I was writing about fat-soluble vitamins for the Weston A. Price Foundation’s journal. And I started the website, which I just recently have started moving over to

    But I started that in 2005. And I think I started my blog, The Daily Lipid, in 2008. So anyway, I’ve been around in the blogosphere and internet for quite awhile. And so there are probably at least a few people in the crowd who know me since back then.

    DrMR: Yeah, I would think most people have probably come across your name, definitely, especially, as you said, regarding vitamin D and/or the other fat-soluble nutrients. And today, I definitely wanted to dig a little bit more deeply into vitamin D.

    Big Picture on Vitamin D

    DrMR: And I guess, do you have any big picture thoughts? And then maybe we can use that to dig into some of the details regarding vitamin D for people listening.

    They may be struggling with, “Somewhere, I’ve read I should be near 100 for my blood levels. I’ve read in other places, that may be dangerous. I’ve read that supplementation is good. I’ve read supplementation may not be as good as the sun.”

    People are probably reading these conflicting things and wondering, from someone like yourself who is grounded in science and pretty reasonable in their approach, do you have any kind of big-picture thoughts as we kind of wade into this discussion?

    DrCM: Yeah, before I do the big picture, just a little-picture thing—I would emphasize that not everyone reports vitamin D in the same units. And 100 could be relatively reasonable or absolutely crazy depending on whether that’s nanograms per milliliter [ng/mL] or nanomoles per liter [nmol/L].

    And I say this only because I’ve been in conversations where people have been reading stuff on the internet that was coming from someone in another country where they primarily used nanomoles per liter. And we have been in discussions. And it has taken us ten minutes to realize that we were talking in different units.

    DrMR: And that’s actually a great point, Chris, because I struggle with that. There was one paper I had read that really I was having a hard time understanding how they could be recommending these units. And then I realized that there are kind of more European-based units or States-based units. So will we be speaking predominantly in the nanograms per milliliter, kind of like the United States?

    DrCM: Yeah, I always—

    DrMR: Okay.

    DrCM: And it’s not just the United States. I guess it depends where you’re getting it measured. But I do some consulting with people from other countries who are getting their units back in nanograms per milliliter. So I don’t know if it depends on maybe they’re using labs in the United States. Or maybe the U.S. influence is spreading. But anyway, I’m accustomed to nanograms per milliliter.

    DrMR: Okay.

    DrCM: So let’s assume we mean that—

    DrMR: And same here, yeah.

    DrCM: Unless otherwise stated, yeah.

    DrMR: Perfect.

    DrCM: Yeah, even in my scientific presentations, it’s usually nanomoles per liter in scientific papers. So I’m always talking to audiences that are familiar with nanograms per milliliter. So in my presentation slides, I usually do a lot of work to change the axis of the graphs if I show data or make a double axis so that people can see where nanograms per milliliter is. Otherwise, it’s incredibly confusing.

    Anyway, so to the big picture, I think. One could start drawing a big picture in many places with vitamin D. But given the reason that you want me on here, I think it makes sense for me to draw the big picture from the perspective of where I have something unique to offer. And so where I’ve really made my unique contributions is in emphasizing the interactions between the fat-soluble vitamins.

    And I think the big picture with vitamin D is many people do need more vitamin D. Quite often, that means that people need to get outdoors more because vitamin D is not the only reason to go outdoors. There are lots of benefits from being outside.

    And so quite often, I think what we see is people need to add some fatty fish to their diet. They need to bias their egg yolks towards pasture-raised egg yolks. They need to get out of the house. And all those things are true.

    But where we can really get into trouble is when we say, “Okay, everyone needs to be supplementing with large, several thousand IU of vitamin D.” And where we really get into trouble is if we just apply that attention to the singular vitamin and don’t pay attention to the background because if you’re not going outdoors and you’re not eating a good diet and then you add a large amount of vitamin D to your diet, you may be the principle case of sort of the worst case scenario where you’re adding a huge dose of one vitamin and may have a very poor status of all its interacting synergists.

    And I think paying more attention to the dietary balance and the well-roundedness and nutrient density of the total diet and the goodness of the total lifestyle, including getting outdoor sunshine, I think is where the emphasis needs to be.

    And where I’ve sort of started expanding that in the last couple of years is paying attention to a lot of nuances about how to interpret blood tests of 25(OH)D which is the principle marker of vitamin D nutritional status that’s being used. And right now it’s being used in kind of a cookie-cutter approach where it’s become routine for the average person to get 25(OH)D screened in a doctor’s office. And if it’s below a certain point, vitamin D capsules are prescribed.

    And I think that we need a lot more nuance in how we interpret the test in general. And we can get into this more deeply. Where that cut off should be is one question. And yes, there’s a lot of controversy where some people say it should be 30. Some people say it should be 20. Some people say it should be 50. Some people say it should be 80.

    But what I would say is, much more importantly, just having a cutoff of a certain threshold below which you just tell everyone to take vitamin D supplements is in itself too simplistic. It’s not just where you draw that line. It’s the fact that the approach is so simple as to draw a line.

    And what you really want to do is take into account many other interacting factors such as, what is this person’s need for 25(OH)D? If it looks a little low, why is it low? Is it low because they have a different set of genetics that causes them to metabolize vitamin D a little bit differently?

    Is it low because they have a disease process that’s using it up? It is low because they have good nutritional status of other synergists that are helping them use it better? Or is it low because they really need more? And you really have to ask those questions if you’re going to give an appropriate treatment to someone, I think.

    Vitamin D as a Marker of Ill Health

    DrMR: I think those are all really very important and very salient remarks (Dr. Ruscio’s Recommended Vitamin D/K Supplement). And there are a few things that I would just like to kind of expand on. To remind the audience, if they want to go back in our archives, we did do a review of the high level of clinical trials using vitamin D supplementation and looked at some of the observational data.

    And in agreement with what Chris is saying, I think, we see a lot of association with low vitamin D and different diseases. But when we just give vitamin D, we don’t really see a lot of favorable benefit in many diseases when we just supplement vitamin D back up to the levels that are observed in healthy persons.

    And this has led many of the high-level, systematic reviews and meta-analyses to conclude that vitamin D may more so be a marker of ill health than it is something that just needs to be strictly supplemented or mono-supplemented upward.

    But there may be a few caveats to that also. We reviewed a couple trials. Oh, and this has just been in the past few months actually. There was one trial showing that vitamin D supplementation helped to lower the antibodies associated with thyroid autoimmunity, the thyroid peroxidase antibodies. And there was recently a clinical trial published showing that vitamin D supplementation had a marked impact on symptoms in IBS.

    So I think there are some nuances. And I think maybe the area where the scientific literature is the most sparse and there may be some discoveries to be made with the utility of vitamin D supplementation maybe with autoimmune conditions. But I think Chris also makes an excellent, excellent point, which is we shouldn’t be looking at vitamin D just by itself.

    And as much of the scientific literature also is asking—is vitamin D a marker of ill health in that person? And it’s maybe a healthcare issue that needs to be addressed? Or is it as simple as just, “Vitamin D is low; let’s give supplemental vitamin D”? And I think in more of the cases, it’s probably something that should prompt further questioning rather than just this reflexive supplementation with vitamin D.

    And I would love to get more of your thoughts, Chris, on—wherever you want to start with how to interpret labs or maybe the best way to look more globally at a person and ask the question, are they vitamin D deficient perhaps because they’re obese? I know that’s been reported.

    There could be an inflammatory issue we’ve talked about. Some have put forth the theory that certain infections can accelerate the conversion of 25 to 125. So I’d be curious to hear if you have any insights there.

    Low 25-OH Vitamin D Levels and Parathyroid Hormone

    DrMR: But yeah, curious to hear your thoughts on interpretation or interventions when we see low vitamin D.

    DrCM: Sure. Well, I guess let’s start with kind of the practical end of this. And usually, I kind of start the opposite way. But let’s start with what I think are the practical implications. And then we can peel apart details of explanations sort of the backwards way.

    DrMR: Sure. Cool.

    DrCM: I think that when you see low 25(OH)D, particularly if it’s moderately low—so as an example, 25(OH)D in the 20s where you are—the Food and Nutrition Board of the Institute of Medicine would say you’re all set. The laboratory reference ranges would say you’re too low. Some people on the internet would say you’re profoundly deficient.

    But I think being in the 20s would be an example of where we could say it’s a little on the low side, but it’s certainly not indicative of a classical vitamin D deficiency where we would see Ricketts or osteomalacia or anything like that. So let’s take that example.

    If you look at white European ancestry populations, you would see that that level is, in general, considered inadequate for a pretty good reason. And that is that in a cross-sectional analysis of vitamin D status and parathyroid hormone, for example, you would see that that amount of circulating 25(OH)D would probably be inadequate to maximally suppress parathyroid hormone.

    And the importance of parathyroid hormone is critical. And it is, in fact, the basis for increasing cut off for adequate 25(OH)D up to 30 or 32 ng/mL in the last decade or so. That rationale is that that’s the amount of circulating 25(OH)D that we would expect to maximally suppress parathyroid hormone in someone.

    And the significance of that is that parathyroid hormone is the body’s natural response to its own perception that it is deficient in calcium and vitamin D. So the parathyroid gland is essentially monitoring serum calcium levels on a continuous basis and initiating a response to slight fluctuations within fractions of a second and actually carrying out a response that will normalize serum calcium over the period of seconds to minutes.

    And serum calcium needs to be so tightly regulated that if someone is deficient in vitamin D or calcium, you won’t see the serum calcium drop at all unless it’s really, really severe. What you will see instead is that that person has equilibrated to a new steady state secretion of parathyroid hormone where parathyroid hormone, or PTH, will be elevated.

    And so you can see that elevation of PTH as the parathyroid—I think of the parathyroid gland as the resident expert in the human body about the vitamin D and calcium economy. And if PTH is elevated in an individual, you know that individual’s parathyroid gland has decided that that individual is deficient in vitamin D or calcium.

    So the whole basis for the bottom of the reference range for adequate 25(OH)D is this idea that, looking cross-sectionally, we see that people who reach that certain point of 25(OH)D have reached a bottoming out point for parathyroid hormone where it has reached the trough.

    Now, one of these sophistications that we need to add is that if you look at someone who is not of white European ancestry, all of these numbers—not the principle—but these numbers go out the window.

    So for example, if you look at Asians, if you look at African Americans, if you look at people of Inuit ancestry—all of these people, even Asians who are living in Hawaii who are young and healthy and get the equivalent of—I don’t remember the exact number but something like 20 hours of full body, unprotected sun exposure a day—Asians in those situations will have 25(OH)D on average in the 20s whereas whites will have it in the 30s.

    And if you look at studies where these other populations have parathyroid hormone levels measured or calcitriol levels measured, which is the fully active, hormonal form of vitamin D, what you seem to see is that there are genetic polymorphisms in—not that every individual has. But on average, there are genetic differences in non white populations that allow them to have higher calcitriol and lower PTH for a lower 25(OH)D.

    So if we were to ask the same exact question by which we defined the adequate level of 25(OH)D for the general population, if we were to exclude people of white European ancestry from that, we would probably recalibrate that number to somewhere in the 20s instead of in the low 30s.

    Now, all of a sudden, if you take that understanding and you stop there, you have a major problem, which is I just potentially gave the impression that all whites will have their PTH bottom out in the low 30s, and all African Americans, Asians, and people of Inuit ancestry will have it bottom out in the 20s. That’s not true.

    What are underlying these things are polymorphisms in the pathway of vitamin D metabolism that, on average, are more prevalent in one group or the other. But still in any group, there are individuals who have one set of genes. There are individuals who have another set of genes. And that means that you really need to treat everyone as an individual.

    And so one of the things that I would advocate to try to get around this is why not take the principle that we are already using on a population level and actually individualize it by looking to see someone’s parathyroid hormone. Why indirectly assess that principle of getting enough vitamin D and calcium to maximally suppress PTH? Why measure that only with 25(OH)D? Why not actually see if that individual person’s PTH is maximally suppressed?

    And I think the real utility of that is that in these—I introduced the idea of genetic polymorphisms helping someone make more calcitriol with less PTH. There are also other cases where 25(OH)D would be low because, for example, supplying vitamin E helps mobilize vitamin D and helps stimulate it getting into the kidney to make it easier to synthesize calcitriol from it.

    And there is considerable evidence that vitamin A and vitamin D actually synergize to increase important health endpoints. So for example, there was an often-neglected but really important study in the 1940s where they took people who had frequent colds. And they gave them large doses of vitamin A alone, large doses of vitamin D alone, or large doses of both of them together.

    And most of the people in the first two groups had to drop out of the study because the people who got vitamin A were getting vitamin A toxicity. The people who got vitamin D were getting vitamin D toxicity.

    But the people who did stay in the study didn’t experience any benefit in reducing their colds, whereas the people who got both vitamins together not only didn’t experience any toxicity, not only stayed through the whole study over the course of several years, but had a dramatic and powerful decrease in the incidence of their colds.

    So if you combine those health endpoints with data from animal experiments, that would suggest that if you have really good vitamin A status, you’re going to improve your utilization of vitamin D and mobilize it more often, use it more often for all these important health endpoint processes. And in that case, you will probably have lower 25(OH)D than someone who doesn’t have good status of these synergists and has vitamin D but just isn’t using it very much.

    And so in those cases, if you consult the resident expert, the parathyroid gland, by looking at someone’s PTH, then that gives you a sense of whether that person’s own body perceives the vitamin D and calcium economy to be adequate.

    And so in cases where vitamin D input is deficient or calcium input is deficient or in the case of an inflammatory disorder where the inflammation is utilizing the vitamin D supply to such a degree that it’s actually taxing the system, any of these things should make PTH rise. And that should be the indicator of how the body is perceiving that economy.

    And when I say rise, what I really mean is rise into the upper half of the reference range. So the reference range for PTH is extremely broad. And it’s based on diagnosing parathyroid disorders. I think if you look at where do people wind up when they’re getting adequate vitamin D and calcium to maximally suppress PTH, that usually means that you’re pushing PTH into the bottom half of the reference range.

    I’m not sure where the exact inflection point is. But it’s somewhere around 30 picograms per milliliter or maybe a little bit higher than that. So if I see someone who’s at 33 or 35, I probably wouldn’t be too concerned. But I think if you’re in the 40s or you’re in the 50s or you’re heading up towards 60 for PTH, then that’s definitely a corroboration that your own body thinks that you’re deficient in vitamin D or calcium.

    DrMR: Those are great points, Chris. So let me try to repeat that as a question to make sure that I’m wrapping my head around this appropriately and also for people listening, how they may be able to do this or ask their doctor to help them walk through this.

    So would it be fair to say that we can personalize one’s dose of vitamin D irrespective of their vitamin D receptor polymorphisms and other factors if we use the parathyroid hormone to guide the dosing?

    DrCM: Yeah, absolutely. And I don’t want to argue here that this is the final answer. What I want to argue here is doing exactly that is a huge step forward—

    DrMR: Sure.

    DrCM: In better interpreting 25(OH)D.

    DrMR: Gotcha. No, it makes complete sense. And just to repeat this again to make sure that I have everything correct on my end, you would titrate up the dose of vitamin D or potentially just keep someone on a given dose for a little while longer and then reevaluate until you see their PTH get to around 30, 35, or roughly the lower half of the reference range for the parathyroid hormone?

    DrCM: Correct.

    DrMR: That is great. That is really, really insightful. And one of the things I did want to ask you about was what your thoughts were on the vitamin D polymorphism, because that seems to be one of the main things that can throw a monkey wrench in interpreting vitamin D as can, potentially, infection or inflammation and how they can accelerate that conversion from 25 vitamin D to 125 vitamin D or calcitriol. And so I think that’s a really novel approach to look at the parathyroid hormone because you’ll kind of cut through a lot of this noise, so to speak.

    DrCM: But it’s almost bizarre that it’s novel—

    DrMR: Right.

    DrCM: Because I’m not even giving a new principle. I’m just saying take the conventional rationale for the 25(OH)D cut point, PTH suppression, and actually look at the individual and see if it’s maximally suppressed. It’s the exact conventional rationale. It’s just individualized.

    DrMR: Sure.

    DrCM: And I think if you actually look at the data that supplies—one of the reasons why the laboratory reference ranges are at odds with what the Food and Nutrition Board of the Institute of Medicine, which is what makes the RDA—part of the reason that they’re at odds about what is the threshold for adequacy of 25(OH)D is because the research is conflicting on what is the level you need to maximally suppress PTH.

    And when they first came out with that highly controversial—at least in the blogosphere—when they first came out with the 2010 RDAs for vitamin D, they gave a conference presentation at Experimental Biology. And I watched their presentation. And they showed a lot of conflicting studies that indicated that the data is actually really messy about what the level is that maximally suppresses 25(OH)D.

    And the messiest thing about it is that it’s not even based on intervention studies where they’re showing how much 25(OH)D do you need to intervene with to maximally suppress PTH in people. It’s just cross-sectional data.

    So they just take a lot of people. They don’t do anything to intervene to change someone’s vitamin D status. The studies just take the cross-sectional data of who has what 25(OH)D and who has what PTH. And if you map that on a graph, you should see a slope downward until you reach a certain level.

    You can follow the line to this maximal suppression. But the variation, the individual data points around that line, is so broad that it’s just obvious from that data that different individuals are responding differently. So it’s bizarre that this is so novel.

    You would think that it follows—or I would think anyway. That’s why I’m saying this—that it follows straightforwardly from that rationale. Let’s actually put the clean version of the story aside, realize that the story is really messy, and look at the individual person and see what’s going on in their body.

    DrMR: That makes complete sense. And there is one thing I’d like to just add in for people that probably goes without saying. But at least as I look at this issue, I can’t help but think if your vitamin D is off, we can look at some of these markers to help guide vitamin D dosing. But also don’t forget that—and as you were saying, Chris, I think this data can be very conflicting because of the individual response.

    And a lot of that may be fueled by other healthcare issues that need to be addressed to make one dose of vitamin D optimum for one person and not optimum for somebody else. If someone has an active inflammatory issue or gastrointestinal malabsorption or an active infection, it’s probably going to make it much harder to sort any of this out.

    So don’t forget about the importance of looking at the overall health picture. And if you have active IBS or IBD or you’re sick often, you’re frequently getting colds and flus, don’t forget about looking into those causative factors, which may be fueled by vitamin D deficiency but may also be fueled by something else. Look at these things in a broader context, not solely to do with the vitamin D levels.

    DrCM: Yeah. Well, while you’re bringing that up, I’ll make one important caveat to this, which is that if someone has a simultaneous magnesium deficiency, it could compromise the PTH response. I think someone has to be pretty badly magnesium deficient for this to happen.

    But if you had someone that had multiple deficiencies going on and the magnesium deficiency was really bad, you could potentially have all of these signs. And yet even the PTH response would be compromised.

    So you always have to look at the big picture. Even with this, I’m not advocating a cookie-cutter approach. You have to take the entire clinical history and the entire set of signs and symptoms that someone is experiencing and the diet and lifestyle and integrate all of that information into a holistic judgment.

    DrMR: Absolutely. Absolutely.

    Vitamin D Polymorphisms

    DrMR: One thing on the vitamin D polymorphisms I’d be curious to hear your thoughts on—I’ve seen some papers suggesting that vitamin D receptor polymorphisms may put one at increased risk for autoimmunity. And I’ve been tracking this issue. And I’ve seen some papers come through.

    And from what I’ve seen, the vitamin D polymorphism hasn’t been consistently implicated as a major corollary to autoimmune disease. So it seems like it may not have a huge hand in autoimmunity. But I’ve only been following this issue for maybe the past year.

    So there may be preexisting data that I haven’t seen roll through. Do you have any thoughts on how the vitamin D polymorphism can affect or increase or maybe not increase someone’s risk for autoimmune conditions?

    DrCM: That’s something that’s been interesting to me and kind of on the back burner. I have looked at some papers here and there. But I haven’t really sat down and hunkered down and intensively researched it like some of the other areas that I have.

    So my opinion is pretty tentative. But I would just point out that if you have—depending on the nature of the polymorphism, presumably if the association is causal, it is because it’s affecting downstream vitamin D signaling. So vitamin D gets metabolized into the active form that can bind to the vitamin D receptor and then do things in the cell.

    And presumably if the polymorphisms in the vitamin D receptor are associated with autoimmunity, it’s not because of the polymorphism per se. It’s because that polymorphism changes what it’s doing.

    DrMR: Right.

    DrCM: So take for example a vitamin D receptor polymorphism that would make it harder for the vitamin D receptor to bind to the hormonal forms of vitamin D or would make it harder for the receptor to bind to DNA. Then the reason it would be tied to autoimmunity is because less total vitamin D signaling is what’s actually tied to autoimmunity.

    But if that’s the case, there are two things. Number one, it would also be the case that in someone without the polymorphism, their vitamin D status would be involved. And then furthermore, in someone with the polymorphism, vitamin D status could modulate the effects. So maybe someone with the polymorphism has a different threshold for 25(OH)D that is needed to support the regulation of the immune system in that manner.

    So in that case, I wouldn’t necessarily expect the association to be clean because it isn’t an association that’s driven specifically by the polymorphism but rather by the vitamin D status that is influenced both by nutritional supply and the polymorphism and what happens after that.

    If I were to spend the time to intensively research this, maybe my answer would be a little bit more concrete. But I wouldn’t expect the association to necessarily be that clean. And I think what we really need to do is start interpreting vitamin D status as nuanced and sophisticated as we can. And then try to define who it is that needs more vitamin D and see whether the polymorphism changes that judgment.

    So to expand on this, suppose that there is a polymorphism in the vitamin D receptor that makes vitamin D less effective at its signaling and makes you need more vitamin D input to get the same vitamin D signaling. In that case, it should also be that in that person, you should need more vitamin D input to maximally suppress parathyroid hormone.

    So if that person requires more 25(OH)D to maximally suppress PTH, then do we need to know the polymorphism? Or can we just look at PTH in that person? I think looking at it this way in research would help us so much because I have never seen a convincing randomized control trial where raising 25(OH)D beyond that point that maximally suppressed PTH had any health benefit.

    DrMR: Sure.

    DrCM: And so if someone shows that that’s the case, then that means that we need to go back to the drawing board and find out what is the next step to better understand this. But if we would just do research studies and classify people according to whether their PTH is maximally suppressed or not and then pick the people in whom it’s not and see what dose of vitamin D has what effect, that would go a long way towards clarifying, do we even need to map out the polymorphisms? Or can we just look at PTH?

    And it would be really nice to know that because this is very complicated. But if we can simplify the complication into a few small tools that can be used properly, everyone will benefit.

    DrMR: Yeah, and you beat me to my next question or my next thought, which was irrespective of the vitamin D polymorphism status, if we’re using this parathyroid hormone as a gauge, might we be able to circumvent that as an issue and get someone to the appropriate dose for them? And I think logic would suggest that would be the case. But it would be great to have a clinical trial looking at that more specifically.

    And along those same lines, it’s funny that you say it’s not really a huge dose of vitamin D that’s needed to get the parathyroid hormone levels into the normal range. And it doesn’t seem that there’s a whole lot of benefit when we supplement people much higher than that level.

    And that correlates with what some of these studies I was referencing earlier showed. The IBS trial I believe used 3500 IUs a day. And the thyroid autoimmunity trial used 2000 IUs a day. So none of these are huge doses that would be expected to really creep someone’s vitamin D level very high.

    So I think that’s important to reiterate, that with some of the clinical benefit we have seen from some of the trials with vitamin D, the dose has not been excessive. It’s been very reasonable.

    DrCM: Yeah, usually when you see benefits in RCTs, you’re dealing with people who have much lower than average 25(OH)D. If they do measure PTH, which they usually don’t, then usually if there’s a benefit, PTH is in the range that you would expect 25 more vitamin D to suppress it. And sometimes, you even have before and after data and see that that is the case.

    But even when they don’t measure PTH, a lot of these trials, you’re bringing someone up to the 20s. Or maybe you’re bringing someone up to over 30 ng/mL. But very often, they’re taking people who have 25(OH)D in the teens. And they’re moving them into the 20s.

    So I would think someone with bad gastrointestinal issues would need a lot of vitamin D just to get their 25(OH)D to anywhere within what anyone would agree is adequate, because if you’re compromising gastrointestinal absorption, then clearly you’re going to need more vitamin D to get that into the system.

    Vitamin D and Sex Hormones

    DrCM: But I want to bring up one thing that came up when I was looking at testosterone. So I was putting together a presentation for Paleo f(x). And I’m actually going to be expanding on this throughout the year at AHS and Wise Traditions.

    But I was looking into the fat-soluble vitamins and sex hormones. And there is one trial that has gotten pretty good attention over the years, where they found that, taking men with low 25(OH)D and low testosterone, vitamin D supplementation increased their testosterone.

    And when I first started looking at this study and reading the discussion and getting a sense of the broader literature around it, my initial impression was, okay, these people have 25(OH)D that is considerably below 30 ng/mL. They’re bringing 25(OH)D up to around the bottom of that.

    So they’re in the inadequate range. And none of the effect is from going from 30 to higher. It’s all from going up to about 30. PTH was measured in the trial. And vitamin D supplementation suppressed it. And testosterone was low.

    And so my thought is, well, okay. What this shows is that when PTH is not maximally suppressed and 25(OH)D is very low and testosterone is very low, that’s when you have an effect. And there are some negative studies out there.

    But as I started looking at the other literature, there were two other papers, each of had three randomized control trials that weren’t designed to test this. But they had archived blood samples. So they went back at those trials and analyzed them to see if there was an effect of vitamin D supplementation on testosterone. And so altogether, this is six additional trials besides this one.

    And none of those trials showed an effect. And in some of those trials, the men also had low testosterone and low 25(OH)D. So in that case, it was really a matter of looking at the total body of literature because you would expect from basic statistical principles, you would expect that if there’s no effect of some treatment and you do ten studies, then you should find one study that shows a positive effect, one study that shows a negative effect, and a bunch of studies that show no effect.

    So if you do one study and you see an effect, what you want to know is what happens if you do ten more studies of that size. And do you see it consistently? Because it may be that there’s an effect. And it may be that it was a fluke. And that’s very possible when you’re dealing with small studies as these usually are.

    The more I looked into the fat-soluble vitamin and sex hormone signaling issue, the more I realized that you probably are not going to get an effect of vitamin D if you’re not paying attention to the synergists. So I looked at men and women and the whole topic of sex hormones.

    And the only convincing study that I found of benefit of sex hormones was in women with polycystic ovarian syndrome, where they were supplemented with a combination of vitamin D, calcium, and vitamin K2. And they didn’t look at that combination versus the individual components.

    So we can’t say for sure that they have to be combined in that manner. But that study showed that androgen levels were significantly diminished in women with PCOS. And in that case, androgens are high, problematically so.

    And that study was much more convincing than any of the singular vitamin D supplementation trials that I looked at. So while I don’t think that the evidence is sufficient for me to come out and say, “We know definitively that we need this particular combination,” I would say that based on everything else that I’ve been researching with the interactions and based on looking at the sex hormone trials, I really do think that quite often we’re not seeing a benefit of vitamin D, not necessarily because there’s no effect but because it’s working in synergy with these other nutrients.

    So it’s not only the case that the person actually has to be in a position where they need more vitamin D, but even in that case, you may not get the benefit that you want to see from the vitamin D unless you take the interactions into account. And so I think it’s always going to be the case that you can’t just focus in on the one nutrient. You really need to do a complete analysis of the person’s diet and lifestyle and try to locate the weak points in that.

    So if 25(OH)D is low and PTH is high, that still isn’t a reason to say, “Okay, prescription 3000 IU vitamin D. Go home, and come back in six months.” The implication of that should be, “Are you getting outside? Are you eating organ meats? Are you eating green leafy vegetables? Are you getting a significant source of calcium in your diet?” And find all of the weak points and fix them. And I think that’s where you’re really going to see the benefits.

    DrMR: I agree. And I think that’s really well said. And it pulls at a principle that I think is really important, which is, it can be tempting to make these things highly complicated and get super lost in the minutiae.

    But oftentimes, the best clinical approach is to zoom out and come back to these more general and broad principles, just like you said, which is looking at someone’s overall diet and lifestyle. And that’s probably going to be the best way to get the system all the many nutrients it needs to be able to function appropriately. So I think that’s very well said.

    And with that, what are some important items for people to be aware of to make sure that they’re getting a good round of nutrients? And I’m assuming you’re looking at this in a kind of focused way with an eye toward the fat-soluble nutrients. But what tips do you have for people to make sure that they’re getting a good balance of all these important vitamin synergists?

    DrCM: Sure. I would say that, first of all, as a general principle, you are only as good as what you digest and absorb. So you need to be eating foods that you tolerate well digestively. If you have digestive problems, you need to work on them. Quite often, that may mean just supplementing with some digestive aids.

    In my case, I’ve had weak digestion all my life. And I actually eat a little bit of raw ginger root with every meal. I don’t think many people would want to do that. But it’s so cheap. And it works so fantastically for me.

    But some people who have problems with fat digestion may benefit from bitters, with protein digestion may benefit from including more umami tastes and so on and so forth. So definitely work on your digestion.

    And definitely don’t be afraid of fat. Fat is needed to absorb all of the fat-soluble vitamins. So those two principles are really beneficial in putting someone in the position where they’re actually absorbing the things that they’re consuming.

    For vitamin D, I would say if you can try to eat fatty fish once a week, if you can try to regularly include pasture-raised egg yolks, it seems that when—we don’t have good rigorous peer-reviewed data on this. But we do have some preliminary data just from farmers pooling their eggs and having them analyzed outside the peer-reviewed literature.

    And it looks like egg yolks, if they’re from pasture-raised chickens, actually compete with fatty fish as a source of vitamin D. So I think just eating some fatty fish and eating some pasture-raised egg yolks go a long way.

    Egg yolks are also providing a little bit of vitamin A. They’re also one of the main sources of vitamin K2. So even just including the pasture-raised egg yolks really goes really far in rounding out the diet.

    For vitamin A, a lot of people can get red, orange, yellow, and green vegetables as a source of vitamin A. But many people—and I’m not talking about a minority. I’m talking about half the population has problems deriving vitamin A from plant foods.

    And so in that case, I would say for everyone, you don’t really know who you are with respect to that principle. So if everyone were to eat a serving of liver once a week, then that would go a long way toward hitting those bases because one serving of liver a week actually supplies the RDA for vitamin A. So even if you had a major problem with getting vitamin A from plant foods, that one serving of liver a week is securing you against any major inadequacy in vitamin A.

    But definitely, the more colorful vegetables you eat, you’re getting an incredible array of other nutrients. So I would say everyone should try to eat some organ meats, especially liver, but should also eat a lot of leaves and a lot of colorful vegetables. That way you don’t need to micromanage and think about all those different nutrients. But just getting that diversity of colors in will go a long way toward getting the diversity of micronutrients that are hiding behind those colors.

    In terms of vitamin K, I mentioned egg yolks. Aged cheese is another great source of vitamin K. If you don’t tolerate eggs and dairy products, then you may want to consider a supplement. Or you may want to eat some more obscure sources of vitamin K2 like goose liver and natto. So the easy way is egg yolks and cheese. The difficult way is goose liver and natto.

    And the fallback is obviously any of these things can be taken in supplements. But I really think that to try to hit the nutritional bases first is best.

    And critical to everything we’ve been talking about is calcium. So vitamin D does many things. But quantitatively, the most important reason that you use up vitamin D is to help control your calcium. And if you are eating a calcium-deficient diet, that’s going to tax your vitamin D supply.

    So I think that a lot of people say, “Well, hey, paleo people didn’t eat dairy products. Therefore, the calcium recommendations are way too high. And I don’t need to worry about it.” But I think if you look at what our ancestors were eating, sure, they weren’t eating dairy products before dairy animals were domesticated in any significant quantity.

    But they were eating insects and insect exoskeletons. Most people are not eating insects anymore. The convenient way to do that, of course, is to eat crickets in the form of Exo Bars right now. And if you look at Exo Bars, look at the labeling. There’s 10% of the RDA for calcium in one bar. And that bar isn’t mostly crickets. Crickets are a part of that bar.

    So if you imagine our ancestors eating 10% whole insects, they’re getting a lot of calcium from that. And if you look at some modern hunter/gatherers—take for example the Hadza—they don’t eat dairy products. But they eat this obscure plant food called—I’m probably butchering the pronunciation, but baobab or something like that. The ethnographers have said that that’s one of their food groups and that it supplies maybe 20% of their calories. And that is—you’re talking milk levels of calcium.

    So I think that people do need to pay attention to their calcium intake. And by far and away the easiest way to do that is some form of dairy product that you digest well. But if you’re not doing dairy products, then try to get insect exoskeletons and bones. For example, canned sardines are a great source of edible bones; same thing with canned salmon.

    And if you’re not doing dairy products, insects, or bones, you’re at the point where you really need to micromanage your calcium intake. So I think if you just take the simple rule of trying to get either dairy products, exoskeletons, or bones, then that sort of takes care of that whole thing.

    And then apart from those specific rules that most relate to what we’ve been talking about, I would just say, try to eat real food. If you cut out most of the junk food, eat mostly unrefined whole foods, and make that a diversity of foods where you’re not heavily restricting any particular group, then you don’t need to think about micromanaging all the different vitamins and minerals. That diversity of nutrient-dense foods will put you in a position where you have that insurance and you don’t need to micromanage it because you are getting a good amount of everything.

    DrMR: No, I think that’s incredibly well said. And I think it’s important to continually emphasize the fact that this stuff doesn’t have to be incredibly meticulous, because what I see in the clinic is patients come in very afraid and thinking like these things are incredibly hard to quantify and to measure and to do. And they almost get the paralysis-by-analysis sort of mentality.

    And it’s always refreshing when we have an expert on here from different specialties. But they all seem to be hinting at similar things, which are the importance of healthy diet and lifestyle and how much we get out of that and how there are exceptions where we have to be a little bit more meticulous.

    But you just gave a great iteration of fatty fish once per week, pasture-raised egg yolks, organ meats once a week, orange vegetables, aged cheeses, maybe dairy if you can do it, insect exoskeletons if that appeals to you, or canned fish with the bone in. That’s fantastic.

    And I think it’s important for people to be reassured that if you eat that way, you’re probably going to be fine. And you don’t have to get super crazy with doing multiple assays over the course of several months and burn through a bunch of money with a functional medicine provider.

    But I do think, back to your earlier point, Chris, that if you have gastrointestinal symptoms and you haven’t been able to resolve those on your own, then it is a very good idea to work with a clinician.

    And of course, I have a bias here, being someone who focuses on gastrointestinal disorders. But that’s definitely one of the first pieces we want to get in order because that will, of course, compromise all absorption. So I love the simplicity in that. And I think that’s really profound.

    The last question I’d like to ask you is regarding sun exposure. It seems from my review of the literature that the best way to obtain vitamin D is through the sun. And also there are vitamin D independent health benefits that you get from the sun that you don’t get from vitamin D. So what are your thoughts on sun and how to factor that in with everything else?

    DrCM: So we are starting to emerge from this era where we only emphasized the negative aspects of sun exposure. And I think those of us who are in the know about vitamin D recognize that the sun has a lot of benefits.

    But I think it’s important to realize that both of those are true. And they’re not mutually exclusive. So it’s absolutely true that ultraviolet rays can cause damage in the body, particularly to the skin. And if you look at human evolution, very clearly, we have had protection from the sun in the form of fur, in the form of dark skin. And the evolution of light skin is relatively recent, much more recent than the emigration out of Africa by current estimates.

    So I think it’s important to realize that you don’t want to go out in the sun and just burn. But at the same time, sun is really important to get vitamin D from. And it’s also really important for setting the circadian rhythm.

    And in fact, if you look at people in equatorial regions who live traditional lifestyles, whether they’re hunters and gatherers or horticulturalists, their peak sun exposure is actually around 9:00 a.m. And that’s because they sleep outside. They get sun immediately upon the sun rising. And then as it gets hot, they seek shade during the midday.

    Now, if you live in a temperate region, then you don’t want to exactly replicate that because for about three-quarters of the year at a latitude that’s far away from the equator, the only time you can get vitamin D synthesis is actually during midday. But that window really widens during the summer.

    So I would say you want to pay really careful attention to the point at which you change color and burn. In general, if your skin has changed color from the sun, you’ve gone beyond the point of maximal vitamin D synthesis. So there’s an aesthetic value to tanning. But you don’t need to go that far to get your vitamin D benefit.

    So I think that if you have really sensitive skin, probably the best thing to do is have a natural, nontoxic sunscreen and get some midday sun. But after you get a little bit of midday sun for your vitamin D benefit, if you’re going to stay out in the sun, begin to follow conventional recommendations about either wearing clothes and a hat that protect you from the sun or putting a natural, nontoxic sunscreen on. And I should say natural, nontoxic, effective sunscreen on, on the areas of your body that are most likely to burn.

    But don’t just think about vitamin D. Also think about your circadian rhythm. We sleep indoors. That is a gross deviation from our entire ancestral lifestyle. So I make it a point now to wake up. I open the windows to get the natural sunlight. I get ready. As soon as I’m ready, I go out for a half-an-hour walk and get morning sunshine. That’s really beneficial to your circadian rhythm.

    And maybe there are lots of other physiological stuff that goes on from the sun. But there’s also just de-stressing. You don’t need an expert to tell you that being in a house all day long or being cooped up in an office or cubicle all day long is stressful.

    DrMR: Sure.

    DrCM: Going out for a walk in a natural environment is really important to get on a regular basis just for relaxing and taking in the outdoors.

    DrMR: Yeah, I totally agree. And I have discussed in a few of the past episodes how one thing that has been a huge kind of well-being cathartic for me has been taking a few breaks during my days where I work at home, getting up from my desk. And I walk outside. And I have a pair of minimal-sole, flat shoes that just feel great to walk in.

    And I get these walks outside. And I get activity. I get light. And I take a break from sitting. And that to me has just paid such huge dividends in terms of my energy and my focus during the day, way more than I’ve seen from adrenal support or all these other things that we try to use for performance aids. And I think that’s really, really important to emphasize just the power of some of these simple things.

    Chris, they discuss in many of the research papers getting enough sun to obtain what they term your minimal erythemal dose, which is enough sun exposure to cause just a slight pigmentation change in the skin, a slight pinkening of the skin. Do you think that’s a reasonable dose? Or are you saying that that’s too much?

    DrCM: Well, I think that’s reasonable because that’s the point at which you know it’s too much. So you’re not going to get any benefit from meeting or exceeding the minimal erythemal dose. But you’re not going to know where the minimal erythemal dose is if you didn’t meet it.

    So I think the reason that that’s used is because it’s a handy tool to actually know where that transition takes place. But if you didn’t reach it and you went just below that dose, I think you would be all set in terms of maxing out your vitamin D synthesis. But how are you going to know where that point is if you don’t meet it?

    So I don’t know that someone needs to monitor their color change necessarily. But I think by the time that you’re old enough to listen to a podcast like this and take it in, you’ve probably had enough experience that you have a reasonable intuitive idea—

    DrMR: Right. Yeah.

    DrCM: Of how sensitive to the sun you are.

    DrMR: Sure. Sure.

    DrCM: So you should have a handle on—and maybe you go through life without paying any attention to your experience. In that case, maybe some medication or something is in order. But you should know, “Oh, it’s really bright outside. In my past experience, I can only last about 10 minutes in this.” And so maybe you go out for five or eight minutes. And then you put your hat on or something like that.

    So I think in a research study, that’s how you quantify it. I think for the average person, you get an intuitive sense of what kind of sort of your minimal erythemal dose is.

    DrMR: Sure.

    DrCM: But you don’t actually precisely measure it, like we were saying, to try to keep it simple, I think the guideline that the average person can intuitively follow is go outside. Know your tolerance for sun. Err on the side of never burning.

    DrMR: Yep, I think that’s very practical and very well said. And one thing I’ll just add in here for people listening who may want some more specific guidelines. I wrote an article and it’s on our website. And we’ll put the link to the article in the transcript associated with this episode, where I extrapolated from the Endocrine Society’s 2014 recommendations for obtaining vitamin D or how to get the acceptable levels of vitamin D.

    And I extrapolated from some of their calculations what you could do to get your vitamin D levels into the normal range via sun exposure if you are vitamin D deficient or what your maintenance dose would be. And I broke it down, not only by that, but also by if you were in a bathing suit or if you were in a T-shirt and shorts because those are both going to affect that.

    So there are some guidelines there for people if they wanted more specifics. But I think ultimately Chris has the best recommendation, which is know yourself. Get some sun. Don’t get enough where you burn. And keep it as simple as that.

    Episode Wrap-up

    DrMR:Chris, where can people learn more from you? You already gave your website earlier. But can you repeat your website and anything else you want to share with people to hear more from you?

    DrCM: Yep, my website is There, I host my blog and my podcast. If you want my blog posts, you just go, or go there and click on blog. Same thing for the podcast show notes. But of course if you want to listen to the podcast, just search your favorite podcast app for The Daily Lipid. And then people can also find me on social media—Facebook, Twitter, Instagram, and Snapchat.

    DrMR: Sweet! And you’re going to be, you said, at AHS this year?

    DrCM: I will be at AHS.

    DrMR: Sweet! So I will see you there.

    DrCM: See you there.

    DrMR: Awesome. Well, thanks again, Chris. Good talking to you.

    DrCM: Yeah, same.

    If you need help determining your ideal level of vitamin D, click here.

    What do you think? I would like to hear your thoughts or experience with this.

    The post How to Determine What Your Optimum Level of Vitamin D Is With Dr. Chris Masterjohn, Ph.D. appeared first on Dr. Michael Ruscio.

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