Be Wary Of Vitamin D Supplementation

[somuch4food]

Lol.

The root cause of AI diseases is an inborn resistance to Vit D, with multiple possible genetic causes.

This resistance can be overcome though with very high doses of Vit D.

The patients are indefinitely in remission because the root cause is addressed.

You would know all this if you actually had taken the time to investigate this treatment, which you obviously didn't.

It seems that you think you hold the absolute truth.

Science on nutrition is still too immature that we can be absolutely sure of anything.

The link I posted mentions that the inactive D3 can take the place of the active D3 thus acting like an antagonist. This results in a reduction of inflammation. That sounds a lot like antihistamines which alleviate symptoms but do not cure the condition.

I think that is plausible because I don't think the body would be able to convert the megadose to the active form. Other nutrients are needed and might get depleted by the megadose.

 

[somuch4food]

Another thread questionning vitamin D: Is Supplemental Vitamin D Safe? "RENAL POTASSIUM-WASTING INDUCED BY VITAMIN D"

 

[nad]

There's nothing to overdo.



As i wrote, there are 4500 auto immune patients who for the past 15 years have lived totally normal lives after suffering from MS and other AI diseases., thanks to daily gigantic amounts of Vit D ( 40.000 to 250.000).



It's a fact.

For how long?

 

[camagunn]

Vitamin D Council recommends 35iu x weight in pounds. This should yield around 50 Ng/ml. I take 5,000 iu -- so for my weight I should get into the 30s.

I don't know how valid this is.

 

[burtlancast]

Hey Burt. Do you have a list of the genetic abnormalities with regards to vitamin D resistance that you mentioned?

From an interview with Dr Coimbra:

"Patients with autoimmune disorders have a genetically inherited resistance against the effects of Vitamin D. This resistance affects the immunomodulatory actions of vitamin D, and is a partial, not a complete, resistance. Due to this resistance these people are predisposed to develop autoimmune disorders.

The exact mechanism of this resistance is not clear yet. There are various diseases linked to genetic mutations in the vitamin D receptor, making these people resistant to vitamin D.

The resistance may also be due to an alteration of the enzymes dealing with the conversion and activation of vitamin D, which are two hydroxylases. So there are many different possibilities: an alteration of the first hydroxylase, of the second hydroxylase, an alteration of the vitamin D receptor itself, and a genetic alteration of the protein that captures vitamin D and carries it along into the bloodstream.

All these genetic alterations may explain the individual resistance to vitamin D and an individual may even suffer from two or three of these issues contributing to his / her resistance to the effects of vitamin D.

This is not just a hypothesis: polymorphic changes in one of the two vitamin D hydroxylases (particularly 1-alpha-hydroxylase), or in vitamin D receptor, or in DBP (vitamin D Binding Protein) have been identified and reported in association with autoimmunity."

 

[burtlancast]

It seems that you think you hold the absolute truth.

Science on nutrition is still too immature that we can be absolutely sure of anything.

The link I posted mentions that the inactive D3 can take the place of the active D3 thus acting like an antagonist. This results in a reduction of inflammation. That sounds a lot like antihistamines which alleviate symptoms but do not cure the condition.

I think that is plausible because I don't think the body would be able to convert the megadose to the active form. Other nutrients are needed and might get depleted by the megadose.

Seems to me you have a horse in this race.

 

[Sourdoughbanana]

I was never anywhere near burning or reddening. I am naturally a little bit tan and was going for lowest amounts. I guess I should've done more. Are you not concerned about skin cancers etc?

I'm way more concerned over vitamin D deficiency, and the natural way to get it is through tanning. Skin cancer prevalence is overblown, a slight bit of reddening will only do a world of good.

@burtlancast thank you for sharing the data on super high doses! Worth reading, especially the part where he destroys the RCT-fanatics, whom I cant stand.

 

[Amazoniac]

From an interview with Dr Coimbra:

"Patients with autoimmune disorders have a genetically inherited resistance against the effects of Vitamin D. This resistance affects the immunomodulatory actions of vitamin D, and is a partial, not a complete, resistance. Due to this resistance these people are predisposed to develop autoimmune disorders.

The exact mechanism of this resistance is not clear yet. There are various diseases linked to genetic mutations in the vitamin D receptor, making these people resistant to vitamin D.

The resistance may also be due to an alteration of the enzymes dealing with the conversion and activation of vitamin D, which are two hydroxylases. So there are many different possibilities: an alteration of the first hydroxylase, of the second hydroxylase, an alteration of the vitamin D receptor itself, and a genetic alteration of the protein that captures vitamin D and carries it along into the bloodstream.

All these genetic alterations may explain the individual resistance to vitamin D and an individual may even suffer from two or three of these issues contributing to his / her resistance to the effects of vitamin D.

This is not just a hypothesis: polymorphic changes in one of the two vitamin D hydroxylases (particularly 1-alpha-hydroxylase), or in vitamin D receptor, or in DBP (vitamin D Binding Protein) have been identified and reported in association with autoimmunity."

"The most consistent, I would even say probably ubiquitous triggering factor in relapsing remitting MS, since we have found almost no exceptions among thousands of patients with autoimmune diseases, is a stressful life event, or a prolonged stressful period–for instance, related to professional or familiar environment. It seems to work very similar in most autoimmune disorders."

glucocorticoid exposure during development

Dysregulation of vitamin D metabolism in the brain and myocardium of rats following prolonged exposure to dexamethasone (not about inulin)

--
T helper 17 cell - Wikipedia

"Th17 cells play an important role in maintaining mucosal barriers and contributing to pathogen clearance at mucosal surfaces, but they have also been implicated in autoimmune and inflammatory disorders. The loss of Th17 cell populations at mucosal surfaces has been linked to chronic inflammation and microbial translocation."​

Multiple Sclerosis (MS) Can Be Caused Quite Easily By Change In Hormones (it's for a good reason)


--
Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy

"Magnesium deficiency and calcium deficiency have some similar symptoms (such as cramping), but magnesium is antagonistic to calcium in many systems. It is the basic protective calcium blocker.
Inflammation leads to excessive uptake of calcium by cells, and is a factor in obesity, depression, and the degenerative diseases.
Protein deficiency is an important cause of deranged calcium metabolism. Vitamins K, E, and A are important in regulating calcium metabolism, and preventing osteoporosis."​

--
Multiple sclerosis, protein, fats, and progesterone

"People with MS have chronically increased production of cortisol. This creates a distortion of protein assimilation, resembling a nutritional protein deficiency. Excessive serotonin and estrogen cause a relatively uncontrolled production of cortisol. A vicious circle of inflammatory mediators and amino acid imbalance can result."

"High quality protein, thyroid, pregnenolone and progesterone tend to correct the underlying pathology. These are antiinflammatory, but they are not immunosuppressive or catabolic."​

--
Vitamin D, Mitochondria, and Muscle

"The two most important enzymes responsible for activation or inactivation of 25OHD, CYP27B1 (1a-hydroxylase) and CYP24A1 (24-hydroxylase), are located in the mitochondria, but there are no data that isolated damage to mitochondria apart from global cell damage or genetic abnormalities are the cause of problems of vitamin D metabolism."​

--
On vitamin D regulation..
Cytochrome P450-mediated metabolism of vitamin D

"Work performed on the 25-hydroxylases over the past four decades in humans and a variety of animal species has revealed that several cytochrome P450 enzymes1 (CYPs): CYP2R1, CYP27A1, CYP3A4, CYP2D25, and perhaps others, are capable of 25-hydroxylation of vitamin D3 or related compounds and thus can be referred to as vitamin D3-25-hydroxylases, it is CYP2R1 that is emerging as the physiologicallyrelevant enzyme [9]. On the other hand, there is no ambiguity over the second step of 1α-hydroxylation or the 25-OH-D3-1α-hydroxylase enzyme responsible, which is carried by a single cytochrome P4501 named CYP27B1 [10,11]."

"The inactivation of vitamin D is carried out by the mitochondrial enzyme, 25-hydroxyvitamin D3-24-hydroxylase first described in the early 1970s and initially believed to be involved solely in the renal 24-hydroxylation of 25-OH-D3 [13]. Work performed over the last 35 years has shown that 24-hydroxylase enzyme activity is the result of CYP24A1 [5,14]. CYP24A1 catalyzes the conversion of both 25-OH-D3 and 1,25-(OH)2D3 into a series of 24- and 23- hydroxylated products targeted for excretion along well-established pathways culminating in the water-soluble biliary metabolite, calcitroic acid or a 26,23-lactone."

"CYPs are classified into two main subtypes based upon their subcellular location: microsomal or mitochondrial; with vitamin D metabolism featuring both subtypes [14]. Both mitochondrial and microsomal CYP subtypes do not function alone but are components of electron transport chains. As with all mitochondrial CYPs, the functional enzyme activity for mitochondrial vitamin D-related CYPs (eg CYP27A1, CYP27B1, CYP24A1) requires the assistance of two additional electron-transporting proteins consisting of a general purpose ferredoxin reductase, a general purpose-ferredoxin and a highly specific CYP (Figure 2A). In contrast, microsomal CYPs (eg CYP2R1) require a single general purpose protein NADPH-cytochrome P450 reductase (Figure 2B). All of the vitamin D-related CYPs catalyze single or multiple hydroxylation reactions on specific carbons of the vitamin D substrate using a transient, heme-bound, Fe-O intermediate. The exact site of hydroxylation, termed regioselectivity, can be somewhat variable with vitamin D related-CYPs, human CYP24A1 being documented to hydroxylate at C23, C24, or C26."

"All CYPs possess a cysteine residue and two other residues near to the C terminus which covalently-bind and align the heme group, in addition to several other domains for interaction with the electron transferring machinery, such as ferredoxin or NADPH-cytochrome P450 reductase."

MULTIPLE SCLEROSIS AND OTHER HORMONE-RELATED BRAIN SYNDROMES.

P450 means "protein that absorbs light at a wavelength of 450."

"Administration of a normal diet supplemented with either small amounts of 1,25-(OH)2D3 or use of a high calcium “rescue diet” largely corrects the mineral metabolism and bone defects seen in the CYP27B1-null mouse [89-92]. Global CYP27B1-null animals given high calcium intakes for several months do show growth plate abnormalities, probably exacerbated by secondary hyperparathyroidism and hypophosphatemia [85,87]. However, tissue-specific knockout of the mouse CYP27B1 gene in chondrocytes suggests that growth plate abnormalities are not merely the result of blood mineral ion defects and that local production of 1,25-(OH)2D3 plays a role in growth plate development [93,94]."

"Immunohistochemistry data from analysis of animal and human tissues has revealed the presence of the CYP27B1 protein in several tissues purported to express 1α-hydroxylase activity (eg skin, colon, macrophage, prostate, breast) [78,4]. Not all studies have supported the conclusion that CYP27B1 is expressed outside of the kidney in normal, non-pregnant animals."

"Despite the fact that the existence of the extra-renal 1α-hydroxylase remains tentative, there has been much speculation about its possible role of this enzyme in health and disease [99-101]. It is now widely believed the enzyme exists in non-renal tissues to boost local production of cellular 1,25-(OH)2D3 in a paracrine/autocrine system. Such a role would suggest that cellular 1,25-(OH)2D3 concentrations in extra-renal CYP27B1 tissues might be higher than in the tissues of the classical endocrine system (eg intestine, bone, parathyroid gland) which depend entirely on renally-synthesized, blood-borne 1,25-(OH)2D3 at concentrations ~10-10M. Cell differentiation and anti-proliferative genes regulated in extra-renal tissues (eg macrophage, colon, prostate, skin) may require higher 1,25-(OH)2D3 concentrations. A role for the extra-renal CYP27B1 is also consistent with the epidemiological finding that serum 25-OH-D levels are associated with various health outcomes from bone health to cardiovascular health. In particular, low serum 25-OH-D levels are associated with increased mortality for colon, breast and prostate cancer; increased auto-immune diseases and greater susceptibility to tuberculosis; increased cardiovascular diseases and hypertension. The presence of CYP27B1 in cells of the colon, breast, prostate, monocyte/macrophage and vasculature could explain why serum 25-OH-D levels are so critical to the normal functioning of these tissues."

"The regulation of CYP27B1 (summarized in Figure 6A) has been a major focus ever since the enzyme’s discovery in the early 1970s [1]. Ca2+ and PO43- ions, probably through the hormones: PTH, calcitonin and FGF-23, regulate CYP27B1 expression through complex signal transduction processes [105,67,106,107], while 1,25-(OH)2D3, the end-product of the enzyme down-regulates its own synthesis at the transcriptional level by vitamin D receptor (VDR)-mediated action at the level of the CYP27B1 gene promoter [106,108,109]. Evidence is also accumulating to suggest that CYP27B1 expression is down-regulated through DNA methylation and up-regulated through DNA demethylation [109,110]. While it is logical to isolate CYP27B1 from the rest of the calcium/phosphate homeostatic system, in practice there is a reciprocity between CYP27B1 and CYP24A1 that suggests that the factors up-regulating one enzyme, down-regulate the other. This is evident in the isolated perfused kidney from the rat fed a low-Ca vitamin D-deficient diet, or low-PO4 vitamin D-deficient diet which is in the 1α-hydroxylation mode, and which over a 4 hour perfusion period after being exposed to its 25-OH-D3 substrate turns off CYP27B1 expression and 1α-hydroxylation and turns on CYP24A1 and 24- hydroxylation [111]. The vitamin D metabolic system seems ideally designed to avoid synthesis of excessive amounts of the hormone and also to degrade the hormone, or even its substrate, by super-induction of catabolic processes including CYP24A1. In the VDR-null mouse, we see a complete breakdown of this auto-regulation process because CYP27B1 is not suppressed by excessive 1,25-(OH)2D3 production and CYP24A1 is not actively stimulated, both steps requiring VDR-mediated events."

"The regulation of the extra-renal 1α-hydroxylase has also received attention over the last couple of decades. What is clear is that the renal and extra-renal enzymes are regulated by different factors: the kidney CYP27B1 by calcium/phosphate homeostatic hormones described above; while the extra-renal enzyme is regulated by tissue-specific factors, including cytokines (Figure 6B). Adams et al [112] has shown that macrophages in the granulomatous condition, sarcoidosis, are driven by pro-inflammatory cytokines, such as γ-interferon, which also stimulate extra-renal CYP27B1 activity, that can cause excessive serum 1,25-(OH)2D3, which left unchecked results in hypercalciuria and hypercalcemia."

Also:

- The Amazing Curative Powers of High-Dose Vitamin D in Aging and Autism - Perfect Health Diet | Perfect Health Diet
- Extrarenal Expression of the 25-Hydroxyvitamin D-1-Hydroxylase​

"Recently, the normal up-regulation of the monocyte/macrophage CYP27B1 system was elucidated [116,117,101]. Toll-like receptors (TLRs) on the cell surface respond to the presence of bacteria (eg M. tuberculosis) with a signal transduction process which results in upregulation of VDR and CYP27B1. Uptake of 25-OH-D bound to its blood carrier DBP, allows the cells to then manufacture 1,25-(OH)2D3, which in turn stimulates VDR-mediated gene transcription of cathelicidin. Cathelicidin is an anti-microbial peptide, which specifically kills M. tuberculosis."

"Stubbs et al [118] have demonstrated the existence of a high VDR-high CYP27B1 subpopulation of immune cells making cathelicidin that can be selected by cell-sorting techniques in CKD Stage 5 dialysis patients treated with high doses of vitamin D3 (40,000 IU/ 2 times per week). Despite the fact that these patients are virtually devoid of circulating 1,25-(OH)2D3 at baseline because of their low renal CYP27B1 activity, vitamin D3 supplementation causes a significant increase in serum 1,25-(OH)2D3, posing the question if this metabolite is of monocyte/macrophage extra-renal origin?"

"Though, CYP24A1 was initially referred to as the 25-hydroxyvitamin D3-24-hydroxylase, work with the recombinant enzyme has shown that it is able to catalyze multiple hydroxylation reactions at carbons C-24 and C-23 of the side chain of both 25-OH-D3 and its hormonal form, 1,25-(OH)2D3 [13,14]. Indeed, our view of the role of CYP24A1 has expanded greatly to suggest that this single P450, alone, is responsible for the 5-step, 24-oxidation pathway from 1,25-(OH)2D3 to produce calcitroic acid, a known biliary catabolite [119,120], as well as catalyzing a similar pathway which starts with 23-hydroxylation and culminates in the 1,25-(OH)2D3-26,23-lactone (Figure 1) [121,122]. In addition, CYP24A1 also efficiently hydroxylates the vitamin D2 side chain of 25-OH-D2 and 1,25-(OH)2D2 to give a more limited series of polyhydroxylated products [123,124]."

"[..]raising 1,25-(OH)2D3 in target cells could trigger CYP24A1-mediated catabolism and thus protect cells from excess VDR pathway activation."

"While CYP24A1 has been clearly established as the key enzyme responsible for vitamin D catabolism, it has become evident that CYP24A1 works in balance with CYP27B1, which is the cytochrome P450 enzyme responsible for converting 25-OH-D3 to 1,25-(OH)2D3 both in the kidney where its role in vitamin D hormone activation was first established as well as in extrarenal tissues where its specific purpose remains to be elucidated. The emergence of the extrarenal 1α-hydroxylase (CYP27B1) as a mechanism for raising the cellular concentration of 1,25-(OH)2D3 [99,100] has refocused our attention on the crucial role of target-cell CYP24A1 as a fine-tuning mechanism to attenuate and eventually reduce its level after gene expression has been modulated. While the renal CYP24A1 enzyme may function to balance systemic 25-OH-D3 and 1,25-(OH)2D3 levels, target-cell extra-renal enzyme probably acts in conjunction with CYP27B1 to "fine-tune" target tissue exposure to 1,25-(OH)2D3 hormone [138] (Figure 6B)."​

 

[somuch4food]

Seems to me you have a horse in this race.

I'm simply arguing against your hypothesis. We can have a healthy debate over this if you're up to it.

I am more on the chronic inflammation bandwagon. So, genetics might play a part, but I can't see it being an absolute. Genetics can be useful to identify predispositions. If you believe more in genetics than in chronic inflammation, that's your stance. I am not saying that you are wrong, I just believe that those fields (nutrition, genetics, inflammation, etc.) are too immature to have uncovered the absolute truth and that we should be careful not to be too radical in our positions.

 

[Sourdoughbanana]

@somuch4food I don’t think anyone is saying genetics are an absolute. They quote a Dr who precisely says they load up on vitamin D for those with unfavorable genotypes

Always keep in mind phenotype >>>> genotype. We benefit a lot from gene testing, the question is how do we treat the information?

It seems perfectly reasonable to me to blame most inflammatory related disease (most disease?) to a sedentary indoor life eating trash. Aka, all things Western lifestyle. Plus bad genetics of course.

 

[Tarmander]

From an interview with Dr Coimbra:

"Patients with autoimmune disorders have a genetically inherited resistance against the effects of Vitamin D. This resistance affects the immunomodulatory actions of vitamin D, and is a partial, not a complete, resistance. Due to this resistance these people are predisposed to develop autoimmune disorders.

The exact mechanism of this resistance is not clear yet. There are various diseases linked to genetic mutations in the vitamin D receptor, making these people resistant to vitamin D.

The resistance may also be due to an alteration of the enzymes dealing with the conversion and activation of vitamin D, which are two hydroxylases. So there are many different possibilities: an alteration of the first hydroxylase, of the second hydroxylase, an alteration of the vitamin D receptor itself, and a genetic alteration of the protein that captures vitamin D and carries it along into the bloodstream.

All these genetic alterations may explain the individual resistance to vitamin D and an individual may even suffer from two or three of these issues contributing to his / her resistance to the effects of vitamin D.

This is not just a hypothesis: polymorphic changes in one of the two vitamin D hydroxylases (particularly 1-alpha-hydroxylase), or in vitamin D receptor, or in DBP (vitamin D Binding Protein) have been identified and reported in association with autoimmunity."

Hmm...Coimbra keeps disappointing me with his answers. His insistence on no studies because of the feels, the bogus 95% stat, and now this basic non-answer explanation. I want to take his findings on this and look at my 23andme and have some corroboration.

I will go see if I can find the actual markers for this vitamin D resistance. I appreciate you giving this interview. I will read it and see if I can find anything useful.

 

[burtlancast]

Hmm...Coimbra keeps disappointing me with his answers.

Have you looked at what his patients are saying ?

8 pages of incredible testimonies.

No one asked for his money back.

Coimbra Protocol Testimonies

 

[Tarmander]

Have you looked at what his patients are saying ?

8 pages of incredible testimonies.

No one asked for his money back.

Coimbra Protocol Testimonies

For sure...I am also apart of the facebook group. Some astounding results.

I also see people struggling with it. I just read an account of someone who has been on the protocol for two years and has not had any results. I read a lot of people who are on it, but struggling with making it right. People comment on their posts saying "Are you taking enough magnesium?" and "Have you tried B2?"

In other words, it's exactly like every other protocol that people jump on where some get great results, some don't get any, and some have bad reactions. Reminds me of "I am drinking orange juice and milk, but having issues." ..."Have you tried the carrot salad?"

Also, stats like "95% success rate" are pure propaganda, increase the placebo effect, and are there to sell the program. He refuses to do studies, and results are spaced over years where many many variables come into play.

I am just looking for hard facts. I am not saying there is not something amazing going on for people with MS...but I have jumped on too many autoimmune hype trains in my time to be fooled again.

 

[somuch4food]

Have you looked at what his patients are saying ?

8 pages of incredible testimonies.

Similar stories from the Paleo world:
https://autoimmunewellness.com/category/articles-2/stories-of-recovery/

The exact mechanism of this resistance is not clear yet. There are various diseases linked to genetic mutations in the vitamin D receptor, making these people resistant to vitamin D.

The resistance may also be due to an alteration of the enzymes dealing with the conversion and activation of vitamin D, which are two hydroxylases.

Dr. Coimbra himself speaks with uncertainty in his interview. Don't get fooled by marketing and propaganda.

 

[burtlancast]

Similar stories from the Paleo world:
https://autoimmunewellness.com/category/articles-2/stories-of-recovery/

And which one of these testimonies involve multiple sclerosis ?...

 

[somuch4food]

And which one of these testimonies involve multiple sclerosis ?...

Here is one: Can You Beat MS With the Paleo Diet?

Your argument is weak. You have mentioned autoimmune diseases in general in many of your posts. You were not focused only on MS. And Coimbert's testimonies include other autoimmune diseases.

We seem to be butting heads pretty hard.

 

[burtlancast]

He refuses to do studies, and results are spaced over years where many many variables come into play.

His results are being replicated by about 120 doctors in all countries of the world.
Kind of strange for someone who refuses to do studies, as you claim, lol.

I am just looking for hard facts. I am not saying there is not something amazing going on for people with MS...but I have jumped on too many autoimmune hype trains in my time to be fooled again.

All his protocol is based on the latest scientific studies linking Vit D dysregulations to AI diseases. There's a mountain of scientific research , a lot of scientific trials, and a host of scientists investigating the link Vit D-MS. You couldn't possibly be more fact-based than that even if you tried.

And are you saying all the hopeless MS cases he put into remission are hype ?

What more proofs do you exactly need before concluding something is genuine as opposed to a hype train, lol ?

 

[burtlancast]

Your argument is weak. You have mentioned autoimmune diseases in general in many of your posts. You were not focused only on MS. And Coimbert's testimonies include other autoimmune diseases.

80% of Coimbra's testimonies involve MS, a significantly debilitating AI disease.

Your testimonies involve other less invalidating AI diseases.

Here is one: Can You Beat MS With the Paleo Diet?

Yes, i've known about Dr Wahl. I wish her all the best with her protocol, and i can't say i've read her book or studied her patient history in detail. But i do have concerns how she looks, compared to how the Coimbra patients look.

 

[somuch4food]

@burtlancast Ok, I am done debating with you. You seem pretty set in your ideas. You can't even admit that there might be other solutions.

 

[burtlancast]

@burtlancast Ok, I am done debating with you. You seem pretty set in your ideas. You can't even admit that there might be other solutions.

Newly Diagnosed Type 1 Diabetes In Remission With The High Vit D Coimbra Protocol