The Science Behind The Coimbra Protocol

Discussion in 'D' started by burtlancast, Dec 25, 2018.

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  1. burtlancast

    burtlancast Member

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    This is an english-subtitled 2014 interview with Brazilian neurologist Dr Cecil Coimbra where he explains the scientific basis of his high Vit D therapy for AI diseases, principally MS.

    I'm joining the text file of all the english subtitles downloaded from youtube.



     

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  2. bzmazu

    bzmazu Member

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    Thanks and Merry Christmas!
     
  3. aquaman

    aquaman Member

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    Is the bit D given orally by liquid?

    Any suggestion of best brands? @burtlancast
     
  4. OP
    burtlancast

    burtlancast Member

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    Well, i've just started supplementing with solid 10.000 UI Vit D (so far so good: it seems to make my joints better), and i honestly have no idea what would be the best brand, or whether liquid would be better than solid.

    But i did read from Dr Coimbra solid forms are OK, as long they aren't out of term.
     
  5. OP
    burtlancast

    burtlancast Member

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    Here's the most interesting part of the interview:

     
  6. GAF

    GAF Member

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    Here is the 2nd most interesting part of the interview regarding Vitamin B2 Riboflavin and its necessity with Vit D supplementation (emphasis mine):

    With regard to vitamin D receptors,

    there are various diseases linked to genetic mutations in the vitamin D receptor,

    making these people resistant to vitamin D.

    The onset of this resistance may be due to the fact that the individual in question has an alteration

    of the enzyme dealing with the activation of vitamin D, which are two hydroxylases.

    The individual may have an alteration of the first hydroxylase, of the second hydroxylase,

    he may have an alteration of the vitamin D receptor that is in the cells, the objective of vitamin D action.

    The individual may also have a hereditary genetic alteration of the protein that captures vitamin D and carries it along into the bloodstream.

    So, there are several genetic alterations that may explain the individual resistance to the assimilation of vitamin D.

    An individual may also need a lot more vitamin D because he's overweight for his height.

    The old people have then a lesser amount of vitamin D receptors in every single cell:

    the concentration of vitamin D receptors in every single cell decreases with increasing age.

    So there are many issues explaining why in some cases a person sees his partial resistance to the effects of vitamin D increased.

    An individual may suffer from two or three of these issues contributing to his resistance to the effects of vitamin D.

    Therefore, we use the final effect of this chain, that is a reduction in the levels of the parathyroid hormone.

    It's a way to avoid having to check what actually is the reason for this resistance.

    It doesn't matter if the reason is this, or that, or if there are multiple concurrent reasons for such resistance to vitamin D.

    By measuring the biological effect, that is the decrease of the parathyroid hormone levels,

    we see the final effect of all these possible issues of resistance to vitamin D,

    and it is a way to optimize our work, to then reach the best biological effect of vitamin D for that individual, regardless of the reason why he has a resistance.

    We simplify the whole by measuring a single biological effect, that is a reduction in the levels of the parathyroid hormone.

    Why is vitamin B2 so important in your protocol?

    Yes, because when we produce vitamin D in the skin or we ingest vitamin D,

    we are ingesting the inactive form of vitamin D, which is called cholecalciferol.

    This cholecalciferol undergoes the action of two enzymes, in a consecutive manner, to be transformed into the final form,

    which is precisely the active form.

    Then, cholecalciferol undergoes the action of an enzyme called 25-hydroxylase, which adds a chemical group

    called hydroxyl in the position 25 of the cholecalciferol molecule,

    turning this cholecalciferol into calcidiol-25-hydroxy-vitamin D,

    which is the one measured in the blood to detect whether or not the individual has a deficiency.

    In turn this substance, 25-hydroxy-vitamin D or calcidiol, undergoes the action of a second hydroxylase, which adds

    another chemical group in position 1. Therefore, this enzyme, which is called 1-alpha-hydroxylase, may be genetically altered.

    Finally, through the second hydroxylase, it is produced the active form of vitamin D, called 1,25-dihydroxy D3

    or calcitriol, which will then produce the final biological effect on the immune system and over all the cells in our body.

    Well, these hydroxylases are depending on vitamin B2,

    not directly, but indirectly,


    because in the stage of vitamin D hydroxylation, enzymes oxidise,

    and to pick up a new molecule, to hydroxylate another molecule, therefore,

    it must be reduced, within a chemically called reduction process. And this reduction process requires the presence of vitamin B2.

    About 10-15% of the general population, worldwide,

    has a great difficulty absorbing vitamin B2. This is another genetic alteration concerning 10-15% of the population.

    In some regions of Italy who have experienced endemic malaria throughout the centuries, since 300 BC,

    this percentage may be higher, it can reach 50% of the individuals concerned

    and these regions are generally corresponding to the Po peninsula, which is the region of Venice and to another region on the west side of Italy...

    Another region that has experienced cases of endemic malaria throughout several centuries, since 300 BC,

    is Sardinia, where there have been cases of endemic malaria throughout the centuries.

    And, apparently, people who had difficulty absorbing vitamin B2 from food were resistant to malaria,

    therefore, the children who had this genetic problem didn't die of malaria in infancy,

    they could become adult and pass on their genes to future generations,

    unlike the children who didn't have this genetic alteration and were subject to malaria.

    So, most of the children, who didn't have this genetic alteration were dying of malaria in childhood

    and couldn't pass on their genes to future generations, reach adulthood and pass on their genes to the next generation.

    So, over the centuries, there has been a natural selection and in these regions of Italy are many more people

    with problems absorbing vitamin B2, that is riboflavin, compared to the rest of the world population,

    where we have about 10 -15% of individuals with this difficulty absorbing riboflavin.

    In these regions of Italy, individuals descended from Italians, who also live in Brazil and are descended from Italians

    coming from those regions of Italy, have a greater chance of being carriers of this difficulty to absorb riboflavin.

    This can contribute to resistance to vitamin D,

    because sometimes hydroxylase, in absence of an adequate level of vitamin B2, will malfunction

    and this will be another factor contributing to vitamin D resistance.

    So, for this reason, to not dose vitamin B2 in all individuals,

    since it is not a test readily available in laboratories and the Healthcare System doesn't cover these tests,

    to not dose vitamin B2, we administer vitamin B2, which is absolutely harmless,

    to all individuals, a dose higher than that normally administered, with the aim to cover that deficiency...
     
  7. Hans

    Hans Member

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  8. Amazoniac

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    - The Amazing Curative Powers of High-Dose Vitamin D in Aging and Autism - Perfect Health Diet | Perfect Health Diet

    "Let’s step back for a moment and think about what would cause health to normalize with super-normal 25OHD.

    Suppose that for some reason, cells were unable to convert 25OHD to 1,25D. What would happen?

    First, cells would have unusually low levels of 1,25D for any given level of 25OHD. Since 1,25D is more than a hundred-fold more active as a VDR ligand than 25OHD, this means that their level of VDR activation would be reduced.

    By how much? In many cells, there seems to be a nearly equal balance between 25OHD and 1,25D activation of the VDR. As one paper notes:

    - High Dietary Vitamin D Prevents Hypocalcemia and Osteomalacia in CYP27B1 Knockout Mice

    "In addition to its central role in the vitamin D endocrine system, CYP27B1 is expressed at low levels in extra-renal tissues, including skin, prostate, breast, and colon (9). It has been hypothesized that extra-renal CYP27B1 generates 1,25(OH)2D3, which then acts locally to regulate Ca metabolism [e.g. suppression of parathyroid hormone (PTH) (10) and activation of Ca absorption (11)] and induce nonclassical vitamin D effects such as the regulation of cell proliferation and differentiation (12). This hypothesis predicts that reduced availability of 25(OH)D3 to the extra-renal CYP27B1 limits local vitamin D signaling and protection, whereas high serum 25(OH)D3 maximizes local 1,25(OH)2D3 production and beneficial effects. This model is supported by epidemiological studies that have linked indices of vitamin D status [i.e. vitamin D intake, latitude, UV exposure, and/or circulating 25(OH)D3] with the risk for various chronic diseases, including osteoporosis and cancer (13), as well as cell culture studies that demonstrate the conversion of 25(OH)D3 to 1,25(OH)2D3 in cell types such as activated immune cells and prostate epithelial cells (14,15). However, an alternative explanation for these observations that has yet to be rigorously tested is that 25(OH)D3 can mediate effects in the absence of conversion to 1,25(OH)2D3 by directly activating VDR. In this model, the high serum concentration of 25(OH)D3 [500–1000 times higher than 1,25(OH)2D3] overcomes its low affinity for the receptor [500 times lower than 1,25(OH)2D3]."​

    If the higher activity of 1,25D is almost precisely balanced by its lower abundance, then a cell’s loss of ability to make 1,25D will cut VDR activation in half.

    So to restore VDR activation to normal levels, you would need to raise 25OHD to double normal levels: 70 to 100 ng/ml. [From normal: 35-50 ng/ml]

    This would fit the cases of the autistic child and of Charles, both of whom reached normal health at around 90 ng/ml."


    "It’s a safe bet that Charles does not have a genetic defect in CYP27B1. If he has a CYP27B1 dysfunction, it must have been acquired in old age.

    What could have created the problem? [] Two possibilities are:
    • Infection with a pathogen that interferes with CYP27B1. Pathogens have evolved ways to interfere with other human proteins in order to suppress the immune response. Since CYP27B1 creates 1,25D which enhances immunity, it would not be a surprise if some pathogen had evolved a way to interfere with CYP27B1.
    • Mitochondrial dysfunction. The enzyme coded by CYP27B1 operates in the inner mitochondrial membrane. Only in mitochondria can 1,25D be created. The “mitochondrial theory of aging” holds that mitochondrial decay is the primary cause of aging. Perhaps in elderly people suffering from mitochondrial dysfunction, CYP27B1 does not operate properly."
     
  9. Amazoniac

    Amazoniac Member

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    - Aligning the Paradoxical Role of Vitamin D in Gastrointestinal Immunity

    "Expression of the VDR depends on the tissue and cell type. In the kidney of vitamin D-sufficient hosts the VDR is expressed constitutively [51]. Calcium and 1,25D are in the livings positive regulators of the VDR in the kidney but not the intestine [51]."

    "Like the VDR, the level of 1,25D is tissue specific. In the kidney, the expression of 1alpha hydroxylase (Cyp27B1) is induced by hypocalcemia and the parathyroid hormone [13,53]. In a feedback loop, 1,25D inhibits Cyp27B1 expression in the kidney and induces Cyp24A1 to eliminate excess 1,25D (Box 1). The immune system can also be a source of locally produced 1,25D; however, the amount of Cyp27B1 made by immune cells is extremely low compared with the amount produced in the kidney [11,13]. In addition, the signals that regulate the Cyp27B1 in immune cells are not the same as those that regulate renal Cyp27B1 [11,13]. Lipopolysaccharide (LPS) activation of human macrophages is required for induction of Cyp27B1 [11,54]. Conversely, LPS has no effect on renal production of Cyp27B1 [13]. In the glasses, human macrophages produce 1,25D when activated with toll-like receptors (LPS) and cytokines [11,54]. Activated T cells are also a source of Cyp27B1 [13]. Immune cells produce 1,25D locally following 2–3 days of activation."

    "When the immune system is in homeostasis, the VDR and Cyp27B1 are expressed at low levels (i.e., absence of infection). In the first several days following activation, the immune system does not utilize or respond to vitamin D [31]. Early post-infection, the macrophages and innate cells that are activated immediately following infection are the first to produce 1,25D. Later the acquired T cells are activated 5–7 days post-infection and then 2–3 days after activation the VDR and Cyp27B1 gene are expressed in T cells. Therefore, it is not until 7–10 days post-infection that T cells express the VDR and are targets for 1,25D-mediated inhibition of proliferation, IL-17, and IFN-γ [36]."

    upload_2019-8-25_20-17-3.png

    "Within a few weeks of infection, the T and B cells clear the infection and antigen is eliminated. If the host is vitamin D deficient, they would still be able to eliminate the infection. Vitamin D-deficient mice cleared C. rodentium infection but with delayed kinetics compared with vitamin D-sufficient mice [14]. Conversely, in IBD the antigen cannot be eliminated and the T cells become chronically activated. In activated T cells, the availability of 1,25D would be essential to inhibit IL-17, IFN-γ, and T cell proliferation. In addition, 1,25D induces T regs that produce IL-10 [33,36]. These functions of 1,25D constrain the chronically activated Th1 and Th17 responses and therefore suppress IBD symptoms [55]. If the host is vitamin D deficient, the Th1 and Th17 cells remain chronically activated [36]. 1,25D is therefore critical for the induction of T regs that together with the direct effects of 1,25D on Th1/Th17 cells restrain the IFN-γ and IL-17 response and resolve inflammation."

    "The immune system is designed to eliminate invading pathogens without causing collateral damage to healthy tissue. Therefore, dampening immune responses post-infection is equally important as initiating the immune response to infection. The benefits of vitamin D in experimental models of S. pneumoniae, P. aeruginosa, M. tuberculosis, D. iokinosis, and malaria were shown to be via the reduction of the immunopathology from the infection and not more rapid elimination of the pathogen [46,47,58]. Vitamin D interventions enhanced the resolution of inflammation in patients infected with M. tuberculosis and 1,25D treatment of peripheral blood mononuclear cells from patients with pulmonary tuberculosis downregulated IFN-γ and cytotoxic cell mediators (perforin, granzyme-B, and granulysin) [59,60]."

    "In the absence of venom/"vitamin" D, the damage from poorly controlled immune activation causes immune pathology while infections are cleared. The same mechanisms whereby vitamin D and 1,25D regulate Th1/Th17 cells in IBD are used to control the resolution of immunity following infection and to protect against immunopathology."​
     
  10. Perceiver

    Perceiver New Member

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    Would be wise to supplement with vitamin D having low 25OHD levels but highish 1.25D and high calcium?

    Context:
    6 months ago my serum calcium was at 11.2 mg/dL, two weeks later got back to 10.6 mg/dL
    A month ago calcium was still at 10.6 mg/dL.
    Rechecked two weeks ago (after taking some low dose vitamin K2 MK7) and this was the result:​

    - 25OHD is in the lowish range (23.5 ng/mL) [lab range 30 - 100]
    - 1,25D in the upper range (61 pg/mL) [lab range 19.9 - 79.3]
    - serum calcium in the upper range (9.5 mg/dL) [lab range 8.6 - 10.2]
    - PTH in medium-high range (44 pg/mL) [lab range 10 - 65]
    - serum phosphate (3,4 mg/dL) [lab range 2.5 - 4.5]
    - ionic calcium (1.22 mmol/L) [lab range 1.05 - 1.3]​

    I am dealing with SIBO, parasites and esporadic fatigue episodes.
    I realize my calcium intake is not great mainly due to SIBO dietary restrictions (no dairy, few green vegetables)
    My naturopath recommends supplementing with vitamin D but I am wary of the implications on my calcium levels.​

    I am trying to understand the interactions between 1.25D, 25OHD, PTH, calcium and immune system, and I have a hard time trying to see how my situation fits in.

    What do you think?
     
  11. Amazoniac

    Amazoniac Member

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