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No medical expert can give ANY REASON why not to fix the 25-hydroxyvitamin D levels of someone sick in anything, except the obvious reasons: “It’s against the narrative”, “I will get murdered by big pharma or lose my job” and “I’m totally uninformed and should work as a journalist or something else that requires no brain”.

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You forgot "fact checker." This is also a job which requires no brain.

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Thank you for sharing this important information!

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Thanks for this excellent write-up. I order a 3-month supply of d.velop to have on hand for helping others and have adjusted our maintenance dose of D3 up a bit, according to the above chart. (I was not charged sales tax for U.S. delivery.) It was helpful to know 50 tablets would work as well, if we needed to split available tablets up amongst the needy.

I don’t recall seeing this information on their site. Do the tablets expire or can they be stored long-term?

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Thanks Mary G and BigT. The d.velop and Fortaro tablets seem to have an expiry date about 12 months after I purchased them. I am not a chemist, but I expect they would retain almost all of their calcifediol content for many years, if retained in their original packaging, especially if kept in a freezer - which is where I just put mine, thanks to BigT's message. I don't know when I will use them - it might be many months or years from now.

The d.velop tablets are in plastic-alfoil blister packs. You will be sick of these after working to pop even a dozen of them out, let alone a hundred. However, they should protect the tablets well.

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I have informed a doc who is in touch with Kory about the need for better guidance wrt early treatment in the FLCCC Early Treatment protocol.

As regards vitamin D in that protocol, it should include a recommendation to give calcifediol rather than D3 for certain groups--the obese, the elderly, those with liver dysfunction (e.g., alcoholics), those with intestinal absorption issues (e.g., Crohns'), those who cannot tolerate fat in the diet, and, of course, those with moderate or severe respiratory illness.

Also, since supplementation with D3/calcifediol can cause an increase in novel arterial plaques, co-supplementation with K2 should be recommended. Then we also have to look at supplementation with magnesium for metabolic reasons.

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If calcifediol level is at 50 ng/ml, then this amounts to 250 micrograms in 5 liters of blood.

If you have 50% absorption, then you would need 0.5 mg of calcifediol.

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I should also mention that supplementing with D3 should be done on a bodyweight basis because adipose tissue competes with the liver for D3, but dosing with calcifediol is the same for all adults with 5 liters of blood.

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Supplementation with D3 may not work for people with liver disease or who are obese. Calcifediol eliminates the need to rely on the liver.

Calcifediol also acts in a timely manner when people have immune events, including vaccination, respiratory infections, cancer flareups, autoimmune flareups, a case of poison ivy (it falls in the autoimmune category), food poisoning, etc.

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I'm not sure if you've seen this article about Th-1 deactivation by vitamin D

"Autocrine vitamin D signaling switches off pro-inflammatory programs of TH1 cells"

https://www.nature.com/articles/s41590-021-01080-3

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Thank you for your work! I just subscribed after I saw your comments on the Substack from Mathew Crawford. It makes speechless to see that calcifediol is not a standard treatment. Several studies from Spain have shown you can reduce the risk of death by more than 80% if you treat covid patients with calcifediol. So most of those who died could still be alive if they would have received this treatment.

I also describe this in my book, in my big chapter about Vitamin D.

I see you are an expert for Vitamin D and I would like to discuss this topic with you. I have been reading thousands of studies about vitamin D and I am extremely interested in this topic. But there are some questions I did not find a response to yet... Maybe you can give me your opinion.

For example, regarding the following question, I also asked Dr. William Grant for his opinion. ( I am sure you know him).

Imagine you are taking 5000 I.U. regularly for years and you have a blood level of 50 ng/ml....

This may lower the risk but still does not prevent all infections by 100%...

Iimagine you get infected with covid now. What would you do? There are several options.

Would you:

-just continue taking 5000 daily?

-take some bolus doses (each like 20.000 to 50.000) of cholecalciferol for some days to increase the level to 70 to 100 ng/ml for example?

-take calcifediol (if available, here in Germany I think it would not be available) to increase the level to 70 or 100 ng/ml...?

Or what would you do? I wonder if taking a bolus dose of vitamin D DESPITE already having a level of 50 ng/ml would still be beneficial or if we can not expect any further effect from additional high doses after we already have 50 ng/ml from regular supplementation?? I found no study which tested that.

Will there be additional benefit if you raise your level from 50 to 100 ng/ml after you realize that you are infected? Or is it not necessary? Could this even have negative effects?

What do you think?

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Hi Max, Thanks for subscribing, commenting and asking a significant question. Its my democratic right to tell you what I think about this, but please don't confuse anything I say or write with medical advice. I am an electronic technician and computer programmer. I know more than probably 99.99% of doctors regarding vitamin D, since I collaborate with leading researchers including Bill Grant and have read the most pertinent research. However, medicine is a huge field, and I know only a tiny subset of what doctors need to know. A doctor has enormous knowledge and experience. If they examine you, they can give you medical advice.

The Quraishi graph https://vitamindstopscovid.info/00-evi/#00-quraishi shows that 50 ng/mL 125 nmol/L is a worthy goal, since it seems that for most of the patients in that research study (morbidly obese people undergoing a Rou-en-Y gastric bypass operation), those with 50 ng/mL or more 25-hydroxyvitamin D had bare minimum risk of hospital acquired and surgical site infections.

There's no downside to having twice this amount of 25-hydroxyitamin D, at least in the short term. (*Maybe* in the very long term, if 100 ng/mL was combined with excessive calcium supplementation, little vitamin K2, little magnesium, old age and some bad luck, some calcification of arteries or heart valves might occur.. I am being deliberately overly-cautious for the sake of discussion.) 150 ng/mL is the level above which toxicity might be a concern: search for toxicity at: https://vitamindstopscovid.info/00-evi/ and in particular the Michael Holick et al. article at: https://vitamindstopscovid.info/00-evi/#chauss . Due to the self limiting mechanisms, to attain 150 ng/mL 25-hydroxyvitamin D requires a very much higher vitamin D3 intake than 3 x what is required to attain 50 ng/mL. See the Ekwaru et al. 2014 graph at: https://vitamindstopscovid.info/00-evi/#05-history .

If you face a potentially deadly infection, I would be inclined to boost a known or reasonably assumed 50 ng/mL 25-hydroxyvitamin D with bolus vitamin D3 or with calcifediol. It is surely safe, if you know you are at 50 ng/mL, to, for 70 kg BW, use a single dose of 10mg 400,000 IU vitamin D3 or 1mg of calcifediol. That might take you to 80 ng/mL, or (at least for calcifediol) briefly over 100 ng/mL, but that is just fine.

I would rather face a serious infection being sure my 25-hydroxvyitamin D level was surely adequate or more, than being on the edge of that rising part of the Quraishi graph.

I am 70kg and take 1.25 mg 50,000 IU vitamin D3 a week. This, plus multivitamins, make it about 7,500 IU / day. I guess my 25-hydroxyvitamin D level is between 50 and 120 ng/mL, most likely between 70 and 90 ng/mL. That's good enough for me. I have not had my level tested for years.

For brevity, the above is written directly, as if it was a fact - but it is just my opinion. Readers should take responsibility for their own reading of the research and the opinions they form, or rely on the judgement of someone else who can understand and evaluate the research properly.

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Further to my reply above, the Quraishi graph depicts immune system failure regarding the primarily bacterial pathogens which cause most hospital-acquired and surgical site infections. Maybe fungi would be involved, but probably not viruses. However, the innate and adaptive responses to these three classes of pathogens broadly operate on similar mechanisms.

We can reasonably assume that the 50 ng/mL works so well because it provides most or all immune cells with sufficient 25-hydroxyvitamin D to run their intracrine and paracrine signaling systems, which enable individual cells to respond to their particular circumstances (intracrine) or to the circumstances of nearby cells (paracrine). See the explanation at https://vitamindstopscovid.info/00-evi/#02-compounds .

The other major benefit of 50 ng/mL or at least generally higher 25-hydroxyvitamin D is that it lowers the risk of wildly dysregulated hyper-inflammatory responses. Inflammation is indiscriminate cell destruction, and it is normally only deployed an a large scale against multicellular parasites. (It is, apparently, a legitimate part of response to some or all viral and bacterial infections, but I have never read an account of why this is so, or whether it really is a good response. Maybe it a normal response for most people, with lousy 25-hydroxyvitamin D levels and no helminth infections, and immunologists assume it is necessary.)

Chauss et al. 2021 (link and summary: https://aminotheory.com/cv19/icu/#2021-Chauss did not know the 25-hydroxyvitamin D levels of the hospitalised COVID-19 patients whose Th1 regulatory lymphocytes (from the patients' lungs) they studied - but these cells had insufficient 25-hydroxyvitamin D for their vitamin D based intracrine signaling system to work. So the cells remained stuck in their pro-inflammatory startup program, never switching to their anti-inflammatory shutdown program, despite detecting the signal (a high level of a complement protein) to do so.

All these patients - and the person in this hypothetical question - can be assumed not to have helminth infections. This means they are much more prone to inflammation than is healthy. Please see the full explanation and the research cited at: https://vitamindstopscovid.info/06-adv/ .

A significant proportion of the population (all assumed to have no helminth infections) suffers serious harm from inflammatory auto-immune conditions. Introducing helminths typically reduces or eliminates the symptoms - even with their typically lousy 25-hydroxyvitamin D levels. Substantially raising their 25-hydroxyvitamin D levels, such as towards or above 100 ng/mL, typically reduces or eliminates the symptoms even while they don't have helminth infections.

If you are facing a disease which might trigger an inflammatory response, it is tempting to think that the 50 ng/mL 25-hydroxyvitamin D level - which evidently enables full-strength vitamin D based intracrine and paracrine signaling in multiple types of immune cells which deal with bacteria etc. - is also sufficient to maximise proper regulation of potentially self-destructive inflammatory responses.

However, the evidence from the auto-immune disease sufferers indicates that in the absence of helminths, significantly higher levels are needed to suppress these unhealthy inflammatory responses.

While I don't suffer from any overt inflammatory disorders - and lets assume is true of the hypothetical person we are discussing - I would not want to find out the hard way that when pushed, my immune system in fact could not properly regulate destructive immune responses, in the absence of helminths, with just 50 ng/mL 25-hydroxyvitamin D. This is an argument for aiming towards 100 ng/mL - and for perhaps going beyond this, or even over 150 ng/mL for a while, without any concerns), rather than assuming that 50 ng/mL would do the trick.

On the 06-adv page, please see the article on the Coimbra protocol and the one which follows it on European doctors treating many patients in this way. The McCullough and Batcheller protocols are similar.

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Hi Robin, thank you very much for your great and helpful response! I just wanted to let you know that I am very busy these days but that I read your comments and that I will still reply in 1 or 2 days! I will reply and hopefully we will also be able to discuss more vitamin D topics.

Have a great day. Greetings from Germany, Max

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Robin, I am sorry that it took more time than I thought. I had much stress and had to finish a project. But it was very important for me to come back, so here I am now. Sorry for the delay. And yes, I know you do not provide medical advice! We are just talking about science. This is just a scientific talk. No medical advice.

So to summarize this, you think in case of an infection it might be reasonable to increase the blood level to 80 or even above 100 ng/m, even if you already had like 50 ng/ml when the infection started. And this is because for some people 50 ng/ml might not be enough to stop or mitigate the inflammatory response.

I know the study which had shown that 50 ng/ml is the most effective level (compared with 30 ng/ml) to reduce an inflammatory response. However, they did not investigate whether a higher level might be even more effective. And it is likely that, as you say, a higher level may be more effective.

There is a study from Seal et al. which showed that veterans who had a level of 60 ng/ml had an almost 50% lower risk of death from covid than those who had a level of 15 ng/ml.

So this shows two things: A high level of 60 ng/ml is effective but it is not always effective enough to save all lives. Dr. Grant told me these 60 ng/ml levels must have been due to supplementation because you can not reach such high levels naturally n the area of this study.

So the question is: If they would have increased the level to, for example, 100 ng/ml, would almost all of them still be alive?

And do you think those who died despite having 60 ng/ml were the ones who did not have helminth infections?

So you believe a "deficiency of helminths" might be outweighed by increasing the vitamin D level to far above 100 ng/ml for a while? If you do´t have helminths, then increasing the level to far above 100 ng/ml in case of an infection might help to prevent the severe inflammatory response?

Regarding Helminth infections, I have to admit I never heard about this before. I will read what you sent me about it. But is there a way to find out if you have helminths?

Regarding auto immune diseases, I also reported about the coimbra protocol in my book. I honestly did not know about helminths. I only knew coimbra´s explanation: Auto immune diseases can come into being by a lack of vitamin D, a resistance towards vitamin D and stress in live.

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I would like to talk with you about many more aspects. Vitamin D is an extremely wide topic and there is so much to discuss. I want to know your opinion about several topics if this is okay for you?

Since I am reading many many studies about vitamin D, sometimes I find controversies that I consider difficult to solve. There are some studies which seem to indicate harm due to vitamin D. These studies make me think a lot and I want to find solutions for it, try to understand the reason for the results, try to understand what we can do to prevent these potentially negative effects. Topics I want to discuss with you include the following for example.

In order to start, please choose one or two of them and thereafter we can go to the other topics. If you prefer this, we could also talk via email.

1. The role of Vitamin D in pancreatic cancer ad prostatate cancer (incidence and severe forms). And also the role of the Vitamin D binding protein in this regard.

I have seen very controversial studies. And this worries me a bit. I want to find out the truth here.

2. A study (preprint( suggests that there is a U-shaped effect of the vitamin D level regarding covid infections. But there may be other explainations for this result. And Dr. Gavies´s discussion of this study was very interesting.

3. It is very important for me to find out why the Vitamin D prophylaxis RCT from Mexico showed a strong benefit (much lower risk of covid infection) although the RCT from UK showed no effect (although in this study they reached a higher vitamin D level than in the study from Mexico).

I also talked about this with Dr. Grant and he had some explanations. Most infections in the UK seem to have occured in the beginning of this study when vitamin D did not have an effect yet because they did not administer bolus doses.

We also talked to Dr. Seneff and she believes it may be due to Glyphosate. Mexico has almost no Glyphosate and UK has Glyphosate. And the activation of Vitamin D is blocked by Glyphosate, according to Dr. Seneff.

I also suspect it might have to due with the vaccines. In Mexico, they had not received vaccines yet during the study period. In UK almost all participants received a vaccine during the study period. I wonder if the vaccines might block vitamin D effects in some way. I mean, we know they suppress the immune system. And so it would nout surprise me if Vitamin D might also be less effective for vaccinated people. But this is just a speculation.

4. There is a RCT from 2019 which showed raking 4000 IU of vitamin D daily for 3 years seems to (very slightly) reduce bone mass if I remember correctly. If you have not seen this study, I can search for it and send it to you.

The problem is that they only received vitamin D and no co-factors, no magnesium, no K2 etc. I would want to see the same study in which they add these co-factors.

However, such a study does not exist.

And I am a bit worried that a long term intake of 4000 IU seems to reduce bone mass... Well, this is strange. 4000 will only take most people to 40 ng/ml or so. And this is a totally normal level (at least in areas like Africa or in closer to the equator in general). So how is it possible that a daily intake of this amount can have this effect? And I also wonder if this reduced bone mass indicates that the calcium from the bones was deposited to the arteries... ?!

Sometimes I think or fear that we are adapted to lower vitamin D levels...

Sometimes I think if we want to try keeping a level of >40 ng/ml, this also may have negative effects because we are adapted to lower levels.

Then, on the other hand we see studies like the one from Seal which shows that veterans in the US were saved by 60 ng/ml.... And of course so many other studies show that levels above 40 ng/ml are very important. Reduced mortality rates, reduced disease risks etc.

So as you see, I am thinking and thinking... This Vitamin D topic is difficult and sometimes very contradictory. I am afraid I am doing something wrong if I permantly keep a summer level of vitamin D in my blood (above 40 ng/ml).

I want to know everything. I know there are so many studies which show very important benefits frim Vitamin D. And these studies are the reason why I take it. But sometimes when I read other studies with some contradicting results, I start wondering and thinking... Overthinking.

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And by the way, I am sorry, I know my English is not 100% correct. This is also because I am trying to write fast. Otherwise it could be better. But as you know, I am from Germany and English is not my main language. Sorry for that.

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At least you don't verbs at the end of sentences put. (I couldn't resist.)

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It looks like the online Fortaro shop is now closed. Is there some other source available?

For questions having to do with skin production of vitamin D, you probably should consult a physicist, as optical angles and UV-B absorption are slightly important. ("slightly" has a hupobolic cough-understated-cough tone)

I happen to be trained in physics and have done research in optics having to do with infrared absorption.

I can discuss angles of incidence, the angel of reflection, indices of refraction, etc.

Did you know that different skin types might or _might not_ have different UV-B absorption even though they reflect visible light differently? At least I haven't seen any research into this question.

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Hi Tom, Thanks for mentioning that the Australian website for 0.01mg calcifediol tablets: https://shop.fortaro.com is not working. Today it shows a basic shopify page. Perhaps this is a glitch which will be fixed. If it is still not working in a few weeks time I will update my web pages and this article.

There could be all sorts of variables with the absorption of ca. 297 nm UV-B light into the required depth of the skin to produce vitamin D3. There are certainly lots of constraints on this regarding the atmosphere, angle of the Sun from the vertical etc. I recall reading somewhere that in addition to melanin absorbing UV-B, there was another compound which absorbed it more, but was not so visible - and that this was found more in the skin of people with dark or black skin.

While I am sure there are psychological and likely physical benefits in sunlight exposure in general and probably exposure of the skin, UV-B damages DNA and so increases the risk of skin cancer, so I do not suggest to anyone that it is a good long-term method of getting enough vitamin D3 to attain the 50 ng/mL circulating 25-hydroxyvitamin D the immune system needs.

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The herdsmen of sub-Saharan Africa typically have 25OHD levels of around 60 ng/ml. I don't know that they have high mortality from melanoma.

Spending time in partial shade allows about a 50% exposure to UV-B compared with normal incidence in direct sun because of scattering of UV-B rays. This means that it takes longer to get the D-production effect (and to get a burn as well) in partial shade. I haven't looked at it,, but possibly partial shade cuts exposure to UV-A significantly, which radiation is what damages DNA.

Keratin is a pigment found in the skin--that may be what you are thinking about.

As regards absorption of UV-B, assuming that the angle of incidence of the radiation to the dielectric surface doesn't exceed the critical angle where there is 100% reflection, that absorption for many chemical substances varies by radiation wavelength and is described by the complex index of refraction for each particular wavelength of radiation. (If your eyes didn't glaze over, congratulations.) The impact of this on vitamin D production is that there needs to be actual measurement of vitamin D production for different skin types. We cannot assume that darker skin necessarily means slower production of vitamin D.

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The "glitch" has lasted for several days.

I had questions regarding Wimalawansa's article

https://www.mdpi.com/2072-6643/14/14/2997/htm

"Therefore, quantitatively and percentage-wise, when taken daily, due to its relatively lower affinity to VDBP, more D3 is available to diffuse/endocytose into target cells compared to 25(OH)D "

First, I couldn't see that the reference [9] said anything about D3 availability. Second, I don't recall D3 having much activity wrt VDRs. Third, the degree of adiposity will affect serum D3, which can result in wide divergence of levels.

If you could ask these questions of SW, I would greatly appreciate it.

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