Dr. Tom Guilliams, our go-to expert for anything related to nutrition research, returns to the Evolution of Medicine podcast for the second part of our Controversies in Nutrition series. Dr. Guilliams has written several books on the therapeutic uses of nutritional supplements.

Our guest opens the discussion by rebutting attempts by major medical journals to discredit nutraceuticals. He breaks down the weaknesses of their research and arguments, along with how the studies are biased and unscientific. He also reviews the limitations of specific nutrient biomarkers, realistic expectations for improving methylation through folic acid supplementation, and how to assess optimal vitamin D levels in individuals who receive plentiful sun exposure.

Listen to this episode if you’re interested in:

  • Why treating based on genetic testing may or may not be beneficial
  • The significance of tracking homocysteine levels in patients
  • When to evaluate methionine levels
  • The NAC controversy between the FDA and Amazon



Controversies in Nutrition Pt. II: Vitamin D, Methylation and More | Ep 283


James Maskell: Welcome to the Evolution of Medicine podcast, the place health professionals come to hear from innovators and agitators leading the charge. We cover the latest clinical breakthroughs in health technology, as well as practical tools to help you transform your practice and the health of your community. This podcast is brought to you by the Lifestyle Matrix Resource Center, who provide a range of options to help you deliver successful, effective, functional, and integrative medicine. To find out more and to get started, go to goevomed.com/lmrc. That’s goevomed.com/lmrc.

Welcome to the podcast. We are talking this week with Dr. Tom Guilliams. This is our Controversies in Nutrition series. We did it last year. We’re doing it again this year. In this podcast, we’re going to talk about MTHFR. We’re going to talk about supplements. We’re going to talk about vitamin D. We’re going to talk about sunshine versus supplements. We’re going to talk about magnesium depletion. There’s a lot of good stuff. Thank you so much, all of you, who put in your questions and fed back to us what you thought were controversies and what you wanted us to look at. That’s where this episode comes from.

Special reminder that tomorrow, the 1st of September, 2022, it’s the beginning of, twice a year, we have open enrollment for our Practice Accelerator. I guess what I can say about it: We’ve been doing it for six years. We’ve helped almost 1,000 doctors and practitioners build their own low overhead, technologically enabled practice. Ultimately, the reason why this is important is because you’re going to hear a lot of nuance in the clinical nutrition here today. In order to practice with that level of nuance, you need time with patients, and you need patients to be educated, you need patients to show up, to pay, and then to be able to have the time to really work with them to reverse and prevent chronic illness.

That’s what the Accelerator is all about. We’ve helped all these practitioners really identify: Who can I help? How am I going to help them? What is going to be my technology stack? How do I educate people consistently so that they know what they’re getting into it, they know why I’m the right person for them? Then, how do you go and find those people in the community? So, really excited.

If you are a practitioner that wants to go out on your own, or if you’re running a practice and it’s not running as efficiently as you’d like, and you’d like to sort of create some automation, check out goevomed.com/accelerator. We have a really great partnership with the Lifestyle Matrix Resource Center this year. So, go there, you can set up a time with one of our team to talk about your own practice situation, see if it’s a fit. Enjoy this podcast. Tom Guilliams is a legend, and there’s a lot of great stuff in here.

So, a warm welcome back to the podcast. Favorite myth-buster, Dr. Tom Guilliams. Welcome, Tom.

Dr. Thomas G. Guilliams: Hey, James. Great to be here.

James Maskell: Really happy to have you back. Yeah, we’ve been asking our community about some myths and some controversies in nutrition. Glad to have you here to talk about some of those. Last year, we talked about fish oil and strontium. So, we’re going to get into some different topics this year. I guess maybe where I thought we could start, over the summer, if you want to take a step back, there’s been some interesting, I guess, papers and position papers on supplements generally. Obviously, when we’re talking about controversies in nutrition, I mean, one of them is that you can get all the stuff that you need from diet. Why do you need supplements? Supplements are dangerous. those kind of conversations that we’ve been having forever. So, what came up this summer that you thought was sort of interesting?

Dr. Thomas G. Guilliams: Well, I mean, I don’t know if anybody saw, but in June, JAMA, I mean, it’s always interesting. I’ve been in this industry for 25 years and it seems like The Lancet, New England of Journal Medicine, JAMA, some, Nature, Science, always has almost like this narrative that they have to keep bringing up every couple years. Some of these papers that, if you think about, nothing happens. Why is it published in such big journals?

So, in June, JAMA published two papers from the US Preventative Service Task Force. These are, they go in and they look at typically cardiovascular risk and cancer risk. And they ask the question, “What’s the evidence that multivitamins, multi-minerals reduce the risks, prevent the risk of cardiovascular disease and cancer?” So, they publish those again. As you’d expect, they just add the last couple years’ worth of data to all the stuff they’ve done in the past. Then they sort of republish the data saying that, “Essentially, there’s no evidence to suggest that taking multivitamins or whatever has a substantial risk reduction on cancer risk.” Although, there is some evidence that multivitamins, even in these studies, multivitamin intake does reduce the risk of cancer, statistically, it’s small, but a statistical benefit.

Then cardiovascular risk. This is usually primary prevention. So, the initial risk versus all, which includes secondary risk. It’s almost always an editorial. It almost always comes along with this. This one in JAMA came along with an editorial entitled Multivitamins and Supplements: Benign Prevention or Potentially Harmful Distraction? So, they’re always trying to bait this idea that supplements are not only neutral or potentially just neutral, but a waste of money. The old one was, obviously, “this is a waste of your money,” is kind of the common thread.

But interestingly, they always add… I’ll just introduce a couple things here, which I think is telling. They always start out with something like, “In 2021, people in the US spent an estimated $50 billion in dietary supplements and dietary supplement industry spent $900 million on marketing.” The idea is, they’re somehow… It’s dirty money. They’ve got all this money. What they don’t tell you is that the pharmaceutical industry in 2020, in the US, sold 425 billion and advertisement was 6.5 billion. If they included those numbers, every time they talked about a drug, then everybody would constantly be thinking that there’s this negative thing.

But even more telling is the beginning of the way they write this editorial. I’ll just quote it. It says, “The appeal of supplements is obvious.” So, they’re setting… This is what we call a classic straw man. “The appeal of supplements is obvious. In theory, vitamins and minerals have antioxidant, anti-inflammatory effects that should decrease the development of cardiovascular risk and cancer.” They’re setting it up by saying, “Theoretically, these should do this. They should reduce the risk of cardiovascular and cancer.” So, if they don’t do this, then that means they’re faulty, they don’t live up to the claim. Of course, you know as well as I do that the FDA tells dietary supplement companies that they must state these products do not treat, cure, or prevent any disease.

On the one hand, by definition, they’re not supposed to cure or treat or prevent anything, but if they don’t cure treat or prevent anything, then somehow they’re a harmful distraction. And so, It’s just kind of frustrating. Of course, if you look deeper into these studies, obviously, these patients, many of them, if they already have cardiovascular risk in their family, they’re on a statin, they’re on beta blockers, they’re on diuretics, they’re on antidiabetic medications, all of which obviously affects their risk for cardiovascular disease and, some of these, cancer. Then, you put vitamin C or a multivitamin on top of that. Of course, in many cases, these patients aren’t even known to be deficient in any of these particular nutrients. And so, again, from an experimental standpoint, it’s really not at all designed to test the value of these compounds.

Then lastly, it’s kind of interesting. They always throw in supplements. Meaning most… If you look at the actual data that’s published in these two papers by the US Preventative Task Force, they’re about multivitamins and vitamins and minerals specifically. But the editorial lumps in supplements, which is sort of this huge… Of course, we know that omega-3 fatty acids reduce the risk for cardiovascular disease, but they don’t mention that. We talk about CoQ10, we can talk about probiotics, there’s all these things that fall in this broader supplement category that just get lumped in these editorials.

So, being in this industry for 25 years, we are used to seeing this on a regular basis. I mean, this reminds me of the whole homocysteine folic acid debate when they really saw this, the clinical trials were showing a lot of benefit. Then, when they did these other clinical trials, VISP, the VISP trial, the NORVIT trial, if you remember back in the late ’90s, early 2000s, and then they said, “Well, folic acid doesn’t work. It doesn’t reduce the risk.” Ironically, FDA doesn’t even consider homocysteine a biomarker of cardiovascular risk today. It’s just kind of odd.

If you’re practicing medicine using, if you’re recommending dietary supplements, multivitamins, minerals in your practice, obviously, often you’re dealing with patients who are deficient in these, but these kinds of papers come out is very frustrating to clinicians to know what to do about it. Especially when somebody walks in and says, “Well, here, you’re just giving me expensive urine, essentially.”

James Maskell: Yeah. Yeah. We’ve heard that a lot. Yeah. I mean, it is really frustrating, obviously, and I guess it’s telling in a certain way that everything has continued to grow in spite of all those things. I mean, you literally have to buy something that says, “This doesn’t do anything on the side.” And yet, the industry continues to grow, more and more people making supplements as a part of their lifestyle. As they start with saying, it is kind of obvious. It’s obvious to my nine-year-old daughter that it makes sense. So, I agree with what you’re saying there, and I think it’s telling. And I think most people have managed to tune some of that out because they know that it works. But at the same time, it’s still this ongoing fight. But do you see any significant changes in the way that supplements will be thought of? Because there’s always that looming over everyone’s heads, right?

Dr. Thomas G. Guilliams: Yeah. Well, I mean, I do like to… I mean, obviously, these papers are a good reminder that dietary supplements, vitamins and mineral supplements in people who don’t have severe deficiencies are not magic. They don’t have specific endpoints. Ironically, even in the drug world, we’ve had years and years of things that kind of shake them up. Like when the Women’s Health Initiative came out and said hormone replacement therapy wasn’t doing what they thought it was doing. Or even recently this whole idea of a rethinking of the serotonin deficiency as a precursor to depression. I mean, sometimes there’s these presumptions that we have that need to be tested and looked at.

But I think the difference that people need to realize is that just because you didn’t cure or prevent cardiovascular risk or an event, I didn’t cure or prevent a heart attack. It doesn’t mean that you haven’t improved the tissue levels, the antioxidant benefits. So, if you look at these things marginally, and that’s why looking at something like homocysteine or some of the other biomarkers that we look at, you can see subtle changes in these biomarkers. And you know, based on the epidemiological data, that you are changing physiology. But whether or not that actually affects within the three or five-month or 10-year window of a clinical trial that you prevented heart attack or a death, that’s harder to prove when you have these subtle nutrient changes.

James Maskell: Yeah. Subtle changes over time is what either creates chronic disease or reverses it. I mean, that’s the whole point of functional medicine. Right?
Dr. Thomas G. Guilliams:
Exactly.

James Maskell: Well, let me get into it because you mentioned the homocysteine thing and you talked a little bit about folic acid. On that topic, we have had some questions on that. How would you determine if someone needs methylation support? And what are some of… Can you go by symptoms? Are there objective measures?

Dr. Thomas G. Guilliams: Yeah. I mean, obviously, the whole… If you go back to the homocysteine-lowering papers, a lot of them more fixated on cardiovascular risk. Then, we saw the movement in our field of people looking at methylation, typically the genetics, the MTHFR polymorphisms. They started saying, there started to be… Obviously, you remember the trend, the methylation trend, everyone was getting their MTHFR genes looked at. Then, they were assuming that if you had certain polymorphisms that you need elevated levels of methylated folate or methylated B vitamins.

A lot of questions became like, “Should we be treating genotype or phenotype?” And I’ve written on this topic, actually I wrote a chapter for a textbook on this. I feel pretty strongly that homocysteine becomes a very, very good phenotypic marker for methylation. If you understand the methylation cycle, most clinicians sort of remember the whole recycling of the one-carbon system. The methylation of homocysteine is one of the few things that the MTHFR gene or the methyl folate does.

So, if we have elevated homocysteine and the question is: What is that? A lot of people like to remember, they say, “Well, the ideal is somewhere around seven or lower.” But if you look in the clinical literature and you say, “Well, why didn’t a lot of these studies work?” Is because a lot of those individuals in those studies only had a homocysteine level of let’s say nine. When they gave them 800 micrograms of folic acid, it only dropped it from nine to eight. So, they really didn’t move people from high risk to a really low risk.

Again, I think that rather than just looking at somebody’s MTHFR genotype, if they don’t have elevated homocysteine, you probably don’t need to aggressively go after a lot of methylating-type compounds. So, even methyl folate or B12, B6, these kinds of things. So, If you have a patient that’s, let’s say, they’re homocysteine is above 11, you could probably be a little more aggressive, and you want to try to get that down seven, eight range. If they’re in the eight or nine range already, you’re probably not going to have a dramatic effect on their risk by loading them up with high levels of methyl folate and B12 and those kinds of things. But probably they should have a good B vitamin or make sure whatever multivitamin they’re using gives them enough folate, B6, B12 to make sure that that homocysteine stays in that level.

I mean, if you’ve got somebody with hyperhomocysteinemia, 15, 20, that’s where you’re dealing with individuals where you’re going to want to be giving them like five milligrams, or even sometimes more for a short period of time, five milligrams of folic acid or 5-methyl folate. I typically recommend the 5-methyl folate for anybody that’s got an MTHFR polymorphism, or anytime you’re in the five milligram range with anybody, you probably should be using the methylated form of folate there. Again, treat the phenotype, not the genotype is, I think, where the data lies.

James Maskell: Yeah, I’m really glad you said that. I remember back in 2017, I saw that, obviously, the consumer genetics was moving a lot faster than the provider genetics. You had a lot of people who were going to get the 23andMe test. Then, I think, showing up in functional medicine doctors’ offices and saying, “Hey, help me, treat this.” I think the provider education wasn’t really there. I think one of the things that I had recognized earlier that year was that what we probably needed to do is to bring some of that learning that you just shared to the community at large, so that people could really understand how to interpret their genetic information.

The way to interpret it is treat the phenotype, not necessarily that, because I know those kind of things become sexy and people want to treat it and they blame everything on it. I’m glad you shared that. I want to go a little bit deeper into that. I mean, can someone, if people take these methylated Bs, can it make them feel worse? And can you over-methylate people?

Dr. Thomas G. Guilliams: Yeah. So, this is a question that came up quite a bit during those years where everyone was putting people on… I mean, methyl folate was probably the one that probably got the most attention. I don’t want to get into the details, but methyl B12 really doesn’t create any benefit for methylation. I mean, I typically tell people using methyl B12, methylcobalamin is probably better than cyanocobalamin, but we can’t really prove that, that it really helps methylation any better. But we did hear a lot of people saying, “I gave people high levels of 5-methyl folate and they were getting brain fog or they were getting headaches, or they were getting unusual, a lot of cognitive-type symptoms.” It was attributed very quickly to over-methylation.

To be honest, I spent a lot of time, in those years, looking for anybody that could prove that you were over-methylating or whatever. I don’t know if that’s what’s going on in these cases that you’re over-methylating, but I would say you may be just increasing these vitamins to the point where something is out of balance and creating some sort of… Typically, these are headaches or some sort of neurological symptoms of some kind. So, I would say, for the most part, I don’t know that it’s over-methylating, but it’s probably unnecessary to give those high doses, especially, again, when the homocysteine levels are not elevated.

James Maskell: Well, it’s interesting you mentioned that, because I know that the homocysteine cardiovascular conversation has been going for a while, but I know they’re now starting to look at it in the context of Alzheimer’s as well. You mentioned brain health there. Can you talk into that? Because, obviously, one thing that happened over the summer was this realization that drug discovery in Alzheimer’s was pointing at the wrong… Pointing at beta-amyloid plaque, when it wasn’t the big deal. And doesn’t surprise me now, obviously, that functional medicine approaches to brain health are working, because they’re obviously a lot more nuanced and thoughtful and root-cause generated. So, where’s that conversation of homocysteine and Alzheimer’s?

Dr. Thomas G. Guilliams: Well, this is sort of one of those unfortunate bystander effects for the research on homocysteine and cardiovascular risk. Because if you look at that, they’ll say, “Well, look, there’s no connection. High homocysteine levels, you can ‘reduce’ them with folic acid, but you can’t reduce cardiovascular risk.” Again, those studies were not designed well for that. But because of that, in mainstream media and the mainstream conventional medicine sort of approach, homocysteine then is, “Well, this is no longer a biomarker of interest.”
But if you go back to the data from those years, there was even a more profound relationship between high, elevated homocysteine levels and Alzheimer’s risk. Also, and in osteoporotic risk. So, osteoporosis. So, if you look at those two areas, actually, those are even more dramatic as far as the quintiles or quartiles of homocysteine and risk for Alzheimer’s and risk for fractures and osteoporosis. So, it really is a biomarker of something more global going on in the body, methylation being obviously one of them. It is kind of a biomarker of methylation capacity. So, I don’t think it should be ignored at all. And granted, maybe the methylation bringing homocysteine down by giving folate, B6, B12, isn’t the only thing that we can do, but it tells us that something is going on.

Now, if somebody has had elevated homocysteine levels for 40 or 50 years of their life because of, let’s say, poor methylation, poor diet and whatnot, just changing, bringing that down when they’re 60 for six months isn’t going to change everything. That’s one of the reasons why just using these biomarkers and assuming that if it’s down, all the risks come down immediately: It doesn’t. Because you have, just like we think of, we have these chronic disease, depletion of physiological resilience, depletion of metabolic reserve, just by changing homocysteine levels, you don’t all of a sudden get back all of the reserve capacity that you lost. So, I think that’s important to understand, these biomarkers are important, but you can’t just change them overnight and decrease the risk that’s there.

James Maskell: Well, that’s one of the reasons why changing those markers with lifestyle change rather than just with supplements is a lot more of a robust strategy because, obviously, there’s downstream, knock-on, positive externalities that occur from that. And one of them might be to reduce the homocysteine level, but there’s going to be many other ways by which they’re valuable. Can you talk to, I guess, what some of the lifestyle strategies might be to reduce homocysteine, if the supplementation doesn’t work, or just generally for improving in health?

Dr. Thomas G. Guilliams: Yeah. A lot of people, they’ll come and say, “Look, I’ve got somebody with elevated homocysteine, it’s 12, it’s 15.” And they’ve given them folate, B6, B12. It hasn’t come down very well consistently. Couple things, from a like… Look at their diet, obviously, elevated methionine levels. If they’re consuming high amounts of methionine in the diet, you could look at that. But from a test standpoint, it’s interesting. If you want to try in those individuals to find out if really elevated—I’m talking 10, 15 milligrams of folate, maybe a 5-methyl folate for like a month—if that doesn’t bring it down, the other thing that you want to consider is the fact that the kidney has to get rid of homocysteine. And homocysteine is conjugated or bound to proteins.

So, it’s bound, and it needs to be dislinked. A lot of people find that if you use N-acetyl cysteine, NAC, which again was a controversial nutrient with FDA and Amazon this last year. But, as far as I know, it’s currently available across the board again. So, N-acetyl cysteine will then cleave off the disulfide bridge that connects homocysteine with the protein. In many individuals, you can’t reduce the overall total homocysteine if you can’t get the kidney to remove it and get it out of the system. And if too much is bound to protein, you need to cleave that off.

But if you look at the overall, physical activity brings down homocysteine. We don’t have a lot of lifestyle-specific remedies because we haven’t been looking at homocysteine. We do know that people that maybe have too much alcohol regularly have elevated homocysteine levels. So, reducing alcohol consumption can do that. So, there’s a number of different things that can be done. But if you’re looking at the diet, too much methylation or too much methionine, I should say, and then low B vitamins. So, just in the diet, if you’re just getting a poor… If you’re not eating a lot of fruits and vegetables in the diet, you’re going to have an elevated homocysteine level, typically, but then look at N-acetyl cysteine as a way to do that.

James Maskell: Okay. That makes sense. Great. Well, look, that’s a good dose on N-acetyl cysteine. We’ve talked about methylation, and we’ve talked about supplements, generally. There’s one topic that I want to get onto because when we put out to our community like, “Hey, what are some controversies in nutrition?” One thing that came up a lot during the pandemic, and I just wanted to make sure that I had a chance to ask you some specific questions, was about vitamin D.

Early on in COVID, there were some graphs that got shared around the internet and I shared them because I care about… I think a lot of us realize like, “Wow, will this be the moment where vitamin D levels get paid attention to by the broader population because of COVID risk and vitamin D?” And so, I guess, there are some questions that have come in from our community about vitamin D levels. Let’s just start with, I guess, the consensus on the appropriate blood levels of vitamin D and what your thoughts are on that before we get into some of these other questions.

Dr. Thomas G. Guilliams: Yeah. I mean, vitamin D is controversial. What’s new? I mean, we see controversies on really both, on multiple ends of the vitamin D spectrum, meaning that the conventional medicine community is always doubting the idea of vitamin D, of course. And within the functional, integrative medicine community, they’ve got a lot of nuanced controversies going on between vitamin D. And so, before I get into this question about what, potentially, because obviously it’s very controversial, what is the optimal level.

You know, when you started looking at the COVID publications, of course, they came out very quick because one of the things that, probably one of the nice things was there’s so many people testing vitamin D because of the broad understanding of how important it is. That’s why we had so much data. We had so much data because we had all these people who were measuring vitamin D, people who were taking vitamin D, and then we had COVID hit, and then we could easily inquire and interrogate the data based on vitamin D levels and COVID risk. Early on, it was COVID susceptibility, COVID severity, and I think it’s fairly clear that low vitamin D levels were bad across the board. They increased your risk for COVID. They increased your risk for severity. They increased your risk for inflammation. Across the board.

But the question is: Where is the line in the sand? How much is the minimum that you need? If you start looking at the literature and the data to suggest: What is a prevention for rickets? And I’m going to talk about in nanograms now, nanograms per mL, that can be as low as 10 or 15. So, if you look at a lot of the databases, they will use 20 nanograms per mL as the measure for the low status for deficiency. Of course, most people listening in this are likely to say, “Well, that should at least minimally be 30.” If we start there at that level, a lot of people will say, “No, 30’s still too low. I want them at 40. I want them at 50. I want them at 60.”

So, I’ve been going back and forth. My take has always been 40 to 60. Then, as you know, there’s a lot of controversy between supplementation, raising your status based on supplementation, versus getting it from sunlight. Of course, the whole sunlight is controversial because now a lot of clinicians are saying, “You shouldn’t get any sunlight,” because of the risk for cancer and whatnot. If you look at the data on what would your vitamin D levels be if you were tanning in a tanning booth or getting out in a sun and getting as much exposure as possible until you basically had a suntan, and you did this every day. What would it stabilize that? It depends on the individual, but it looks to be somewhere between 50 and 70, around in there. Obviously, there’s some people that go a little higher for short periods of time, but it stabilizes typically around 50 to 70. So, a lot of people-

James Maskell: We have some of those people in Florida who are out there every day. They may be pushing 80.

Dr. Thomas G. Guilliams: Well, remember, they’re going to get more and more tan. So, it’s going to eventually reduce that amount. Now, a lot of people think that they’re going to get vitamin D when they just walk outside dressed like I am with a T-shirt and pants. For the most part, you’re not going to get much vitamin D from your face and your arms. You really need to expose your torso, as much of your torso as possible, and your legs, because obviously you have to have a lot of skin exposure to get that conversion.

At this point, I would say that I’m kind of coming to a place where I think 60 nanograms per mL is probably the level of close to optimum or where we might think of an optimal. If you look at the status needed, let’s say, to limit autoimmune diseases, it’s usually around that 60 range. I just don’t see in the literature that there’s any other benefits really going up much above that at all. For, I mean, the audience, I don’t know if they realize that most of the vitamin D3 that we get in a supplement is actually from lanolin, it’s from wool, the lanolin and wool, which has the same precursor as our skin. Then you hit it with UV light and you convert it to the same previtamin D3. Then you can use that and make that into D3 as a supplement.

The reason that your body doesn’t get much above 60 or 70 when you’re in sunlight is because eventually the UV or radiation will degrade the previtamin D3. So, it doesn’t just keep accumulating because there is a light-induced degradation process. It’s sort of self-limiting. Obviously, if people are taking too much oral vitamin D3, they can get too much. So, you can get over 100, you can get over 120. There seems to be no benefit, and there potentially is some negative. Most of the curves that you see in the literature are either U-shaped or J-shaped, where eventually the risk that goes down seems to flatten off usually around 60 to 80, and sometimes the risk for cancers or cardiovascular risk starts going up when you get vitamin D levels above that. I mean, it’s hard to know why exactly, we don’t have the exact mechanisms, but it does seem like when we get above 60, you’re probably not going to get much more benefit. That’s kind of where I think we should probably stop.

James Maskell: Okay. Yeah. That makes sense. Your thoughts on supplementation versus getting in the sunlight, I mean. Am I taking from your experience that, if you can get it from sunlight, get it from sunlight? But in some cases, you can’t.

Dr. Thomas G. Guilliams: Yeah. I mean, obviously, depending on where you live, if you’re living in sunny California, like you, you have a better chance than living in Wisconsin, like me. So, I think, this is sort of the controversy, Michael Holick has had to deal with this his whole career because he’s been studying the sunlight and vitamin D. And the dermatologists and everybody really frown upon sunlight at all, seems like. But the other benefits, there’s actually other compounds, the conversion of 7-hydroxy cholesterol into vitamin D or vitamin D3. There are other compounds that are also modified by UV or radiation that actually produce anti-cancer or other benefits in the skin. There’s other benefits we get that we don’t quite understand. When sunlight hits the human skin, it does all kinds of things. It changes our mood and probably there’s a physiological reason it does that.

The recommendation that is typically given by Holick and others, I generally agree with, that if we can get vitamin D—and you can make 20,000 IUs of vitamin D in a short amount of time, if you’re exposed to the right amount of sunlight, to get that amount—that is way below that what would cause you to have a sunburn or whatever. Then, once you have that amount of sun, then put on whatever you need, your hat and your shirt or your sunscreen. Because sunscreen will block the conversion of vitamin D like 90% to 95%. I mean, you can pretty much almost eliminate all the benefits of vitamin D conversion with sunlight using sunblock. Usually, the idea is get that sunlight first, maybe for a half an hour, depending on the time of day and the time of year, and then put on your sunblock after that, if you want to get that natural benefit. But I would say, again, it’s not just vitamin D, there’s probably a lot more going on there.

James Maskell: And steer clear of Banana Boat sunscreen. Right? Hey, just one more thing on that. Obviously, there’s a role for early morning sun in your circadian rhythm, too. Obviously, there’s sort of a knock-on effect and it’s all interrelated, I guess.

Dr. Thomas G. Guilliams: Right. And there, you don’t need to have the sunlight on the skin directly, but you obviously… That’s more hitting the optic nerve and the suprachiasmatic nucleus signaling.

James Maskell: Yeah. Well, look, when I post about vitamin D online, 95% of people are like, “Wow, this is great. Finally.” But then, I always get a few DMs from people, who’ll be like, “No, you’ve got it all wrong. This is totally wrong.” I guess, one thing that came up in those DMs was that vitamin D can cause a drop in magnesium levels and that should be avoided because of the importance of magnesium and all the different things it does in the body. Is this controversial? What do you think about that? What does the literature say?

Dr. Thomas G. Guilliams: So, these are the kind of things that are hard to pin down. Yeah, ironically, most of these people, and I hear the same things you do. And I go online, and I try to figure out: Where is this source of the information coming from? Because I’m a researcher> I want to find out what is actually being referenced. And almost nobody references what they’re talking about. So finding, investigating back to where some of these things… For instance, you’ll see high doses of vitamin D deplete magnesium. High doses of vitamin D deplete potassium. And then that causes a change in all these effects.

So, I kind of investigated: What is the relationship between vitamin D and magnesium, specifically? But there’s probably similarities with other minerals and maybe even other vitamins. So, you got to take a step back and understand that when you read something and you read it in a certain way, it can be interpreted a number of different ways. If you go back to the days of just calcium, we used to tell people—and we still do that—the USRDA, or your need of calcium, is 1,000 milligrams or 1,200 milligrams. Or some people would even say 1,500 milligrams a day. Of course, there’s a whole controversy about diet versus supplements and a whole bunch of other calcium and creating risk for cardiovascular disease.

But behind the scenes of all of that was that question about, “Well, what about vitamin D?” If you give somebody 1,000 milligrams of calcium and they have no vitamin D, their body treats that calcium very different than if they had adequate vitamin D levels. Well, as it turns out, magnesium is required or in the process of taking previtamin D, hydroxylation. Of course, we have to go through two hydroxylation steps to get the 1,25-Dihydroxy vitamin D. That process requires magnesium. So does… Magnesium is required for binding of vitamin D to its vitamin D receptor.

So, because of that, people have said, “Well, if you are going to give somebody so much vitamin D that they need to convert to the active forms, you’re going to deplete their necessary magnesium.” That’s a logical idea. As it turns out, when you actually look into the literature and see what is the relationship between magnesium levels before and after high-dose vitamin D supplementation, you’ll find there’s no evidence that it drops. That’s partly due to the fact that there’s a lot of complicating… And it’s all very controversial as another topic of what is the right way to measure magnesium levels. Is it serum levels? Is it RBC levels? Is it electrolytes? How would you measure the magnesium level? I don’t want to get into that because I don’t know that anybody’s really solved that to the satisfaction of everyone.

But what I would say is this. Somebody that has, let’s say, a vitamin a D level of 30, and we’d say, “Okay, that’s at the bottom of what we would consider adequate.” They might not be getting the full benefit of that vitamin D status if their magnesium status is low. So, they might think, “Well, I need to keep raising. I need to get more vitamin D, more vitamin D.” That extra vitamin D is probably not going to do them nearly as much good as just raising their magnesium levels to adequate amounts, so they can use the vitamin D they already have adequately.

So, I think what we have here is not an issue of, “Am I over-consuming vitamin D?” But if I have inadequate magnesium levels, all of that extra vitamin D is not going to do me a hill of beans. It’s not going to do me a lot of good. So, just like we see with high calcium levels with low vitamin D, we’re seeing the same thing with high vitamin D levels and low magnesium. So, I would suggest that what those individuals should do is say, “Yes, there’s a relationship between vitamin D and magnesium.” But it’s not this knee jerk: Your vitamin D is depleting your magnesium. It’s that your magnesium is not helping your vitamin D. You need to increase your magnesium levels. And I think that’s probably across the board as important, in many cases, as vitamin D levels in people. Magnesium deficiency is probably more globally problematic as well as we see with vitamin D.
That’s probably also true of potassium, maybe some other as well. Iron levels, there’s maybe a connection with iron. But probably the strongest is with magnesium. I would say, people, when they’re going to the literature and they see the fact that magnesium is needed so much for vitamin D, they make the mistake of saying vitamin D depletes magnesium. Actually, ironically, vitamin D increases magnesium absorption. So, it actually could be the other way around. But what you really want is active vitamin D, balanced vitamin D. And in order to get that, you need adequate magnesium levels.

James Maskell: Great.

Dr. Thomas G. Guilliams: So, it’s just like anything like we have in the past, any nutrient can be out of balance and not helpful. And you can’t generate a benefit just by going higher and higher and higher because there’s these other vitamins. That’s how I would answer that question. And I think we still need to know more because there’s very little research in this area.

James Maskell: Well, Tom, look, I’m really glad we were able to talk about that. And hopefully this is valuable for people in the community who are dealing with these kind of questions. If you have questions, feel free to get in touch with us here at Evolution of Medicine, and we can do as best we can to get those questions answered for you. We will continue to do these Controversies in Nutrition podcasts because ultimately there is still a lot of controversies out there. Tom, we’re super grateful for you to come and share your knowledge with us, and I’m grateful for this masterclass in those topics.

So, thanks so much, everyone, for tuning in. This has been the Evolution of Medicine podcast. As I mentioned at the beginning of the show, tomorrow, September 1st is the beginning of open enrollment for our Practice Accelerator. So, check out goevomed.com/accelerator if you’re interested in finding out more about that. If you want to practice this type of medicine, you need time to be able to do it. You need time to work out the nuance just of what Tom was talking about right then. And we are helping doctors make that shift to having time with their patients. Thanks so much for tuning in and we’ll see you next time.

Thanks for listening to the evolution of medicine podcast. Please share this with colleagues who need to hear it. Thanks so much to our sponsors, the Lifestyle Matrix Resource Center. This podcast is really possible because of them. Please visit goevomed.com/lmrc to find out more about their clinical tools like the group visit toolkit. That’s goevomed.com/lmrc. Thanks so much for listening and we’ll see you next time.

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