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Vitamin D dosing varies with genes, PTH, Mg, Vit K, etc – video and transcript Sept 2022


Interpreting Vitamin D Levels (LGS Protocol = Leaky Gut Syndrome)



0:00:25.0 Dr. Beltran: Hi there everybody, this is Dr. Beltran. So here we are for part two of the video. I had promised you guys that we were going to be discussing how we interpret our vitamin D levels, laboratory levels, and how this could have an impact on how our autoimmune diseases behave. Just reminding you guys that vitamin D is actually a hormone that we make in our body. It's made through exposure to the sun. It has different phases of metabolism. It starts at the level of the skin, then it goes to the liver, it gets metabolized into what we know as 25-hydroxyvitamin D. And then finally, there's a conversion at the level of the kidneys where it's transformed into the active metabolite, also known as calcitriol, which is the actual hormone. Once again, our immune cells and many different parts of our body and many different cells of our body have the same enzyme that helps transform 25-hydroxyvitamin D into calcitriol, which is the actual hormone. Intracellularly, they do have an enzyme that does this for them. And this has been proven and it's been shown. And we also have receptors for cholecalciferol and also receptors for calcifediol.

0:01:32.2 DB: But the active metabolite that does a lot of these good things for us is actually calcitriol, which is the actual hormone. So having that said, it's important for you guys to recognize that vitamin D or the hormone D, which it should be called a hormone, calcitriol, has many different genes that participate in the regulation and the synthesis of this hormone. And it's really important for us to recognize what genes participate here and at what level they're found that have a dramatic effect in how our immune system is going to behave, how our gut is going to behave when we're exposed to inflammatory proteins that we get from our diet sometimes, and these genes are easily studied. You can do genetic testing. One of the platforms I would like to use is called SelfDecode. It has changed a little bit recently, the way how the platform is set up and the way you can pay a little bit extra and it'll give you some extra information. It's relatively not as expensive as many other out there. I think it runs for about $200, maybe a little bit more if you get the better version of it. But still, the data is there.

0:02:55.0 DB: And here's the most important thing is that it not only gives you your genetic coding, but it also gives you a whole lot of information in regards to what we call single nucleotide polymorphisms, which are SNPs, which are genes that have a different way of expressing themselves and which differentiates us many times in different categories and many different groups. Some people have blue eyes, some people have brown eyes, some people have blonde hair, some people have dark brown or black hair. In the end, we are all different in a sense and we're also classified into groups. But sometimes these genes, these polymorphisms may be attributed to environmental factors, dietary factors that women that are pregnant, unfortunately are not aware that they were supposed to be taking specific supplements throughout their pregnancy, and this ends up affecting a part of our genetic coding known as our epigenome. And methyl groups are very important here because they help silence sometimes some of these genes that might be problematic down the road and cause some form of autoimmunity for kids. So methylation is a very important component in the regulation of autoimmune disease. And when we don't give women that are, during their pregnancy, we don't give them the adequate amounts of certain vitamins such as vitamin B9 or vitamin B12 in the methyl form, or vitamin D which is very, very important.

0:04:38.8 DB: And having said that, we know that vitamin D, methylfolate, methylcobalamin, they have an important impact in the methylation cycle and they also help in the production, not only in the production of DNA as we know that that's very important, but also the production of methyl groups. And these methyl groups are going to be added on specific endpoints of genes which are going to be able to silence the expression of a bad gene, let's say. Me and you, all of us, we have a total of 23 chromosomes from our mother and our father and they're parallel, one aside each other. Sometimes we might have a good gene here and a bad gene here and this bad gene, in order for it not to be expressed, we add a methyl group to it. Alright? So that's one of the ways how our body tries to maintain equilibrium, homeostasis and also make sure that we don't express certain specific genes. Now, when we don't have adequate methylation, we see issues evolve and arise and the good thing is that these are things that we can actually kind of control in a way through an anti-inflammatory diet, through the supplementations of certain vitamins and minerals and amino acids and especially the most important thing is through diet.

80% of immune system is in gastrointestinal tract.

0:06:06.7 DB: Diet has a profound effect on how our immune system behaves. Let us not forget that 80% of our immune system is found in gastrointestinal tract. So this means that everything that you put into yourself, everything that goes into you is going to have a direct interaction with your immune system. And let us not forget that the gastrointestinal lining, which is made up by a small series of cells known as enterocytes, have a mucus layering on top of it that's known as the mucin layer that isolates the microbiome from interacting with the lamina propria, where our immune system is found, right? So when we start having a thinning of this mucin layer, there's more interaction between the microbiome and also the immune system, thing that should not be happening in the first place. That's why we have this mucin layer in the first place, to be able to isolate one environment from another. But if we have a diet, for instance, that's very poor in fiber, and I'm talking about good fiber, I'm not talking about bad fiber because people think, oh, wheat is a good source of fiber, rye, barley, oats, they're a very good source of fiber. Yes, they do have fiber, but it's not a good fiber because these are lectins, and these lectins are pro-inflammatory.

Glyphosate is an antibiotic that kills your microbiome

0:07:31.5 DB: And not only that, but let's not forget a lot of these food sources, a lot of these grains, they're just infested with glyphosate. They just put a whole bunch of glyphosate on these crops, and you're actually not just putting into yourself an inflammatory lectin, which is going to cause a lot of inflammation inside of the gut, but also you're putting inside of yourself glyphosate, which is actually an antibiotic. Glyphosate was patented back in 1996 as an antibiotic and kills your microbiome. So we're doing a lot of harm, and not only that, it's not just an antibiotic, but it also is cancergenic. It's been proven to have a cancergenic role. So this is why it's always good to go organic, and try to eat a source of fiber that's not dependent on wheat or these grains that I just mentioned like barley, oats, rye, or wheat itself. There are many other sources out there. Avocados are rich in fiber, spirulina, which is an algae, is rich in fiber as well. We have hundreds of different options out there.

Vitamin D genes: CYP2R1, CYP27B1, CYP24A1

0:08:44.6 DB: Anyways, going back to what I was saying, so we have these vitamin D genes that are very important. We have genes that are responsible in the process of the conversion of vitamin D. Here we have two genes, very important genes, known as CYP2R1, which is a gene that helps in the conversion of cholecalciferol into calcifediol, and calcifediol is also known as 25-hydroxyvitamin D. Then we have another gene that helps in the conversion of calcifediol, also known as 25-hydroxyvitamin D, into calcitriol, which is the actual hormone, also known as 1,25-dihydroxyvitamin D. Long names, I know. So this enzyme that's upregulated through a gene, the gene that is called CYP27B1, makes another enzyme that converts calcifediol into calcitriol, known as 1,25-dihydroxylase, is an enzyme that's going to convert calcifediol into calcitriol. Then we have genes that are responsible for the transport of the metabolite, and this is known as a vitamin D binding protein gene, or VDBP gene. Then we have our final destination, which is the vitamin D receptor gene. These are genes that are going to upregulate vitamin D receptors on the surface of the cell and also inside the cell.

0:10:10.9 DB: And this is where the vitamin D metabolite is going to act upon, and it's going to upregulate transcription, and it's going to end up making any type of protein, any type of enzyme that the body requires perhaps down the road. And then finally, we also have a gene, it's known as CYP24A1, which helps in the degradation of calcitriol. So whenever we have too much calcitriol circulating in our body, our body breaks it down in order to make sure that we don't get any type of toxicity, if that's the case. So these are genes that are responsible in the metabolism of vitamin D. Now, one of the things that I've always mentioned, and this has been discussed and also put out in the medical literature, there's a lot of research on it, this is not me inventing these things up, patients who do have autoimmunity have vitamin D gene polymorphisms, and not only vitamin D gene polymorphisms, but they also have polymorphisms in genes that regulate the methylation cycle, such as the MTHFR gene, which needs to be compensated in order to have a good methylation cycle, alright?

Magnesium and a gene: TRPM6

0:11:25.9 DB: And also, we also have patients that have polymorphisms can affect also the genes that regulate how magnesium is transported from the extracellular space into the intracellular space of the cell. So this gene is known as TRPM6, and we do have genetic polymorphisms in regards to this. And do not forget that vitamin D, in order for it to be able to be activated, requires magnesium as a cofactor. Magnesium is so important, it's so important, it participates in more than 300 different enzymatic reactions in our body. It is that important, we need magnesium for everything. There isn't a biochemical reaction that does not require magnesium as a component. So we must make sure that these patients have adequate magnesium intake. And magnesium, when we take it orally, it isn't very well absorbed, unfortunately. So sometimes we need to double up a little bit on the dose and the type of magnesium that we are taking. Then we have different forms of magnesium. We have glycinate, we have citrate. We have more than five different types of magnesiums out there and each of them have their own characteristics. But going back to what I was saying, magnesium is a very important mineral that is essential for many enzymatic reactions and it is a cofactor for vitamin D activation.

Magnesium, Vitamin D, and Vitamin K all regulate Calcium

0:13:00.6 DB: So this is very, very important for you guys to understand. Also, magnesium regulates calcium metabolism in our body as well, such as vitamin D does. Magnesium makes sure that that calcium that we have in our bone doesn't escape the bone, so it prevents you from getting osteoporosis or osteopenia. And also, there is another vitamin that is very important, a liposoluble vitamin, which is vitamin K2, especially the MK7 form. MK7 form is better than the MK4 version of it because it has a longer bioavailability, it has a longer half-life, in other words. And what I wanted to say is this, is that vitamin K2, one of the main functions that it has is that it gets that calcium that you have in the blood or inside of those arteries, and it takes it out and it sends it back into the bone. So in order for us not to have any type of toxicity secondary to high doses of vitamin D therapy in patients who do have autoimmune disease, we always combine magnesium and vitamin K2 together. And obviously, a whole bunch of different other vitamins that are very important because let's not forget that we want to make sure that we have a healthy methylation cycle, we want to make sure that that mitochondria, which is the energy source of every single cell, is functioning well.

SIBO = Small Intestinal Bacterial Overgrowth

0:14:32.7 DB: We also want to make sure that our liver is functioning very well. This is the reason why I always introduce alpha lipoic acid. Alpha lipoic acid is excellent for the liver. It enhances liver metabolism in phase one, two, and three and also we want to make sure that we are assisting the gut. Many of these patients who have autoimmunity have what we call dysbiosis. And sometimes dysbiosis, it can be very severe or it can be moderate or it can be mild. But according to the severity, it can sometimes even cause a condition known as SIBO, which means Small Intestinal Bacterial Overgrowth. Or you can have SIFO, which is a Small Intestinal Fungal Overgrowth. And when this happens, sometimes it's necessary to actually give a form of antibiotic, a natural herb antibiotic. I like to use a lot of licorice sometimes. I also use berberine as an excellent source for killing certain microbes and funguses like candida and oregano oil. Oregano oil an excellent antibiotic. I've been using it for many years and I've seen tremendous results with it. But this is when you actually study your patient, you do the microbiome testing, you do a GI map on these patients, and you notice that there is actual dysbiosis.

0:15:56.9 DB: And not only it's about killing these bad bacteria, but also making sure that the good ones are an adequate amount. Sometimes we need to add on a probiotic to make sure that those good bacterias are getting there. And I always do a little bit of testing to see if we have adequate pancreatic enzymes. One of the enzymes I like to test for is elastase-1. And if I do see that there is a reduction in elastase, I will add on some digestive enzymes to be able to help out in the digestion of certain foods. So the diet that I like to introduce to these patients is an anti-inflammatory diet that's basically characterized by four things. It's gluten-free, and gluten is a lectin. It's dairy-free, because dairy also has lectins. One of them is casein, and a lot of patients do not tolerate casein very well. And there's also lactose, and some people are lactose intolerant as well. And a third group is a group of lectins of foods that are very rich in lectins. And here we have the nightshades, for instance. And fourth, foods that are low in sugar, so low carb. When you do this type of anti-inflammatory diet where you're reducing the consumption of gluten, you eliminate. It's a restrictive diet where you eliminate gluten, you eliminate dairy, you eliminate lectins, and you eliminate excessive amounts of sugars, you start giving that gastrointestinal tract time to be able to heal.

0:17:33.6 DB: Like I had mentioned in the first video, whenever you consume, let's say, gluten, gluten is made out of lectins, and one of those prolamins, lectin-prolamin, is known as Gliadin. Gliadin, when it gets absorbed by the enterocyte, upregulates a protein known as Zonulin. Zonulin breaks the bond existing in between both of these enterocytes. This bond is known as the tight junction. And guess what, calcitriol, when you have adequate and you optimize the levels of calcitriol in these patients, you inhibit zonulin, so in a sense you are actually preventing that tight junction from breaking off. Because calcitriol inhibits zonulin. So going back to what I was about to say, I know this is a long introduction, but I had to get these things out of the way. So going back into how can we compensate these polymorphisms, these genetic polymorphisms in our patients. Well first of all, we have to see what the baseline is, where our patient is at. So I usually, whenever I measure vitamin D metabolites, I always measure 25-hydroxyvitamin D, which is calcifediol, and I measure calcitriol, 1,25-dihydroxyvitamin D. And I always compare these two. If I see that my patient has a low level of 25-hydroxyvitamin D and low levels of calcitriol, that just means that they're vitamin D deficient.

Increase vitamin D dosing until the PTH goes to the low of the reference range

0:19:06.3 DB: It does not tell me if they're actually... They have a genetic polymorphism. So if I start giving them a higher dose of vitamin D, I would usually start up around 40,000, maybe perhaps 50,000 International Units of vitamin D a day. And I do a follow-up in about 30 days to be able to check and see how those vitamin D levels are going up. And I always compare them to a antagonist hormone, which is the parathyroid hormone, and also check their calcium levels, just to make sure that I'm not causing toxicity. So as you guys know, vitamin D, whenever it's low, your PTH, this is PTH and this is vitamin D, is always going to be high because these guys are antagonists. But as soon as you start elevating vitamin D, PTH starts to go down. So one of the main goals in the treatment with high doses of vitamin D is that you try to inhibit and get this guy, PTH, down over to the lower reference levels, and optimize as high as you can your vitamin D levels. And obviously, always making sure that we're not causing harm. And one of the ways we do this is by measuring two forms of calcium.

0:20:23.1 DB: One is known as serum calcium and ionized calcium. So we know that the definition of vitamin D toxicity is when we have hypercalcemia. So if we are giving vitamin D and we are inhibiting PTH, once we reach the lower reference levels, that's usually when we start seeing the patient going to remission because we're optimizing vitamin D levels. But if there is no hypercalcemia, you can say that there is no toxicity, because the definition of vitamin D toxicity is when we have the presence of hypercalcemia. There's no other way of being able to define it. So having that said, I measure my vitamin D levels, once again, after 30 days. And if I start seeing that my 25-hydroxyvitamin D has gone up, and I can barely see an increase in calcitriol, which is 1,25-dihydroxyvitamin D, that kind of starts telling me that there is a problem in the cascade of conversion and perhaps this patient might have a genetic polymorphism in the gene that converts calcifediol into calcitriol. And we know that that gene is known as CYP27B1. So this is an indirect form of being able to measure genetic polymorphisms through laboratory testing.

Sometimes need to treat the gut to lower the PTH

0:21:51.4 DB: So I keep on checking my PTH. And if I notice, let's say, my vitamin D is right over here, and my PTH is still elevated, that means I need to add more vitamin D to that patient. So when I start adding more vitamin D and I see that there's still no toxicity, calcium levels are still being maintained, and then once I start seeing that that PTH starts to go down, that means that I've reached a breaking point. That means that the vitamin D resistance that that patient has, has been broken and now I can start shifting that PTH and trying to inhibit it to the lower reference values, which is basically our main goal. And that's what the Coimbra Protocol teaches us. We try to inhibit PTH in order to achieve remission. Those are one of the goals. But here is a small detail that I always want to say. It's not just about inhibiting PTH, you have to treat the gut as well. If you do everything in regards of treating, compensating those polymorphisms, those genetic polymorphisms, that's great, but if you don't treat the gut, I mean, it's all a lot of work done in vain.

Gut may need a change of diet, herbs, probiotics, etc.

0:23:12.2 DB: So you really need to change the patient's diet, which means you need to go on a gluten-free diet, you need to be dairy-free, and you need to be lectin-free, and you need to be sugar-free. This is essential. And sometimes it's not just only just treating the diet, changing the diet, going on an anti-inflammatory, sometimes you actually really need to treat with antibiotic herbs such as berberine, oregano oil, licorice or whatever, based on your GI map of your microbiome. So going back to our lab. So I said initially we had low levels of 25-hydroxy, low levels of 1,25-hydroxyvitamin D. And then I started giving, let's say, 50,000 International Units. And then I see an increase in 25-hydroxy but a very small increase in calcitriol, which is suggestive of a polymorphism of the gene of CYP27B1, which converts calcifediol into calcitriol. And I see that there hasn't been much of a shift in regards to the PTH level, so this means that I need to increase my dose on vitamin D. And obviously, always making sure calcium is normal, within normal parameters. So you increase your dose, let's say from 50,000, you went up to 80,000.

0:24:32.7 DB: And now you start seeing that calcitriol is trying to get up there too and it's now found within normal ranges, laboratory ranges, which are considered adequate. And obviously your calcifediol, your 25-hydroxy vitamin D, it's going to be way above normal reference range. And this is something that you're going to see. You're going to have to have 25-hydroxyvitamin D that's way above normal reference range, laboratory reference, and a calcitriol that's going to be in what we consider the good zone, normal reference range. You want it to be in the middle. And you don't want it to be close to the lower limit, we want to be kind of like close to the upper limit. And always watching PTH and watching calcium at the same time. You're going to start seeing that PTH starts to go down, go down, go down, go down. That means that you're beating the vitamin D resistance. And calcium itself has to be within normal reference values in order to avoid that toxicity. Sometimes, you'll find that patients don't even respond, not even to one, neither to higher doses. And that might be too many different factors. One, you have to see if the patient is not obese, you have to see if the patient is not taking any medication that's inhibiting vitamin D conversion.

Many drugs reduce Vitamin D levels
Vitamin D stimulates is a co-factor in serotonin production, which makes melatonin

0:25:57.4 DB: We have drugs out there that can actually degrade vitamin D, like steroids, prednisone, glucocorticoids, they degrade calcitriol. A lot of patients who were put on immunosuppressive drugs like steroids, unfortunately, they're depleted in vitamin D because this destroys literally your calcitriol levels. Patients who are taking medications for depression such as antidepressant medications such as fluoxetine inhibit the gene that converts vitamin D. So you will be vitamin D deficient thinking that you are okay. I mean you might be feeling okay because it kind of simulates, it imitates serotonin receptors, it stimulates serotonin receptors but vitamin D is a co-factor for the production of serotonin. Isn't that interesting, huh? I'll repeat it again, vitamin D is a co-factor for producing serotonin and once you start making serotonin, you make melatonin as well. So you're going to not only feel better but you're also going to sleep better. Recall a little bit of biochemistry. Tryptophan gets converted into serotonin. Calcitriol comes over here as a co-factor, stimulates an enzyme that's going to convert tryptophan into serotonin. Same thing goes for dopamine. Dopamine uses tyrosine, calcitriol comes over here as a co-factor and helps in the conversion of tyrosine into dopamine. You see?

Active disease process if calcitriol is high and 25-hydroxyvitamin D is low

0:27:31.7 DB: So calcitriol or vitamin D in general is good for mental health in general. It's good for your gut health. Vitamin D has more than 80 different functions in your body. Alright, let's go back again to the laboratory interpretation. So sometimes you'll also see patients, for instance, that have very high levels of calcitriol, and low levels of 25-hydroxyvitamin D. And whenever I see this, this basically suggests that the patient has active disease process, ongoing active disease process. And the reason why is that we have to remember the half-life of vitamin D. Vitamin D has a half-life. Cholecalciferol, the vitamin D3 that you buy at the store is known as cholecalciferol has a half-life of 24 hours. Calcifediol now has a half-life of 3 weeks, which circulates around your body. It's your body's reserve of vitamin D in order to be able to metabolize it and quickly convert it into calcitriol, if it needs it. And once calcifediol... Calcifediol has a half-life of 3 weeks, I said that. So once this gets converted into the active hormone, calcitriol only has a half-life of only 2 hours, which is nothing, you know?

Need to take vitamin D daily (he is unaware of how it is stored in the body)

0:28:54.8 DB: And this is the reason why you have to be taking vitamin D on a daily basis in order to have continuous levels of calcitriol throughout the day. You need to be taking vitamin D daily. Vitamin D was not made to be consumed on a weekly basis, monthly basis. You can probably maybe perhaps get away with once a week, but still, you're going to be ticking down that reserve. So what happens is that these patients who have autoimmune disease, in order for the body to be able to continue with the demand, the metabolic demand of vitamin D, it needs to burn really quickly that reserve in order to make adequate levels of calcitriol. And so this is why whenever you do some laboratory testing and you see that the patient has elevated calcitriol levels, but low or normal reference levels of 25-hydroxyvitamin D, is suggestive of active disease process.

Sarcoidosis is a form of lymphogranulomatose disease

0:30:00.3 DB: Now, there are some conditions that might actually be included here and I'll tell you which ones they are. Any form of lymphogranulomatose disease can cause this as well. So we need to investigate this. And finally, an example of this you could have is like sarcoidosis. Sarcoidosis is one of those diseases that it can cause hypercalcemia. So we're going to be a little bit careful when we see patients who have that. So those are one of the things I'd like to share with you guys. I hope this information is something that might help you guys, open up a little bit your eyes and maybe perhaps help someone out over there. All righty. It's a pleasure to talk to you guys and see you until next time. Bye-bye.

Added in emails to VitaminDWiki Dec 2022

One thing I forgot to mention is that I do genetic testing and identify the vitamin D genes SNPs that the patients have. I also look at many other genes also MTHFR, MTT, etc. I also use Omega 3 in the protocol. I use more than 15 supplements based on the genetic profile the patient has. I am well aware of how vitamin D is stored in the body... But the requirements vary greatly from one individual to another. I basically apply the basic concepts of the Coimbra Protocol. But I have found that in many patients that the vitamin D dose does not always have to inhibit PTH nor does the vitamin D dose need to be very high in order to obtain remission. Diet is extremely important here! if you watch my mechanisms of autoimmunity I explain this. It truly is a complex subject and the approach must always be multidisciplinary. Autoimmunity has multiple causes. Vitamin D SNPs are just a part of the puzzle.

When using high-dose vitamin D Therapy for autoimmune diseases I always check for the patient's 25OHD and 1,25OHD, PTH, and Ca+ levels before initiating supplementation. Usually, they all have a low vitamin D level prior to treatment. Knowing this I start off with 35.000 to 50.000 IU a day and check once again after 1-2 months. If I see that Calcitriol levels are within mid-reference laboratory levels in the absence of hypercalcemia and notice a shift in PTH levels then I know that I've reached the vitamin D resistance breaking point. Obviously, this must always be correlated with signs of clinical improvement. Now the LGS Protocol is not just about giving vitamin D... It's much more complex than that. Usually, patients have dysbiosis/SIBO/SIFO which needs to be addressed. So the Protocol addresses many contributing factors that promote autoimmunity.

High Dose vitamin Therapy is one of the main components of the therapy. I have a video that briefly talks about this, called Mechanisms of Autoimmunity. In this video, I also explain a concept that I describe as VDR Cleansing through Anti-inflammatory Diet. A true cause of vitamin D resistance. Its well known that Lipopolysaccharides, bacterial toxins, and mycotoxins have high affinity for VDRs. This is a major contributor of vitamin D Resistance due to blockage of the VDR binding site to 25OHD or 1,25OHD. The patient may even have high levels of circulating vitamin D in the blood but little benefit is gained from the active metabolite (calcitriol) due to VDR blockage. When Leaky gut syndrome is addressed less entry of LPSs, toxins, and mycotoxins enter the body and allow for the upregulation of new VDRs. This is the reason why patients improve after going on an anti-inflammatory diet.

VitaminDWiki - Genetics chart shows the vitamin D genes

in Visio for 2023

VitaminDWiki - Calcitriol category contains

56 Calcitriol items in VitaminDWiki     See also: Calcidiol category listing which has 46 items

Many ways to increase Vitamin D - click on chart for details

VitaminDWiki - CYP27B1 category contains

The CYP27B1 gene activates Vitamin D in the Kidney,    Skin,    Lungs,    Brain,   Eyes   Breasts   etc.
Poor CYP27B1 is assocated with COVID, Miscarriage,   Lupus,   Alz, Parkinson, MSA,   Rickets

CYtochrome P450 family 27 subfamily B member 1    = 25-Hydroxyvitamin D3 1-alpha-hydroxylase

What can be done if have a poor CYP27B1

  • Larger doses of Vitamin D
  • More Bio-available: Gut-friendly form, Topical form, taken with fatty meal, taken with evening meal
  • Additional sources: UV
  • Increase Vitamin D metabolism: additional Magnesium, Omega-3
    • All cytochrome P450 enzymes require Mg++ as a cofactor
  • Increase the amount of Vitamin D in the blood that gets to cells: increase activation of VDR

Vitamin D blood test misses CYP27B1 and other genes
in Visio for 2023

VitaminDWiki - Comparing High-dose vitamin D therapies


VitaminDWiki- see also

CYP24A1 gene and Vitamin D - many studies
Sarcoidosis (rare) problems when taking vitamin D - many studies
Melatonin and Vitamin D - many studies
Vitamin D Cofactors in a nutshell
PTH and Vitamin D - many studies 34+ as of Dec 2022
44+ Transcripts in VitaminDWiki
Glyphosate and Vitamin D - many studies
600,000 IU of Vitamin D helped 26 out of 28 COVID-19 patients in ICU (Brazil and Bolivia) June 2021 Beltran

Attached files

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