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The Science Behind The Coimbra Protocol

burtlancast

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Jan 1, 2013
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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.



How was your protocol born?

The protocol emerged from the following question:

in a particular moment of my professional life,

I strongly felt a need to try to help change this idea

that neurology is a medical specialty made by brilliant diagnosticians

but without any effective treatment available for neurological illnesses.

It was considered in this manner in the medical field: a specialty of brilliant diagnosticians

yet one without any effective treatment.

When I finished my clinical training in Miami in the United States at Jackson Memorial Hospital

I returned to Sao Paolo with the idea to specialize and

begin to do research using laboratory animals

and create models of neurological illnesses in rats with the objective to test

new diagnostic possibilities.

In research, we are obligated to be at the forefront;

one cannot simply read neurological textbooks and studies from 5 or 10 years ago;

one must know what is been published last week

that is relevant to the research one is doing.

This was our objective.

Possessing an enormous quantity of research that has not been published in textbooks,

we asked ourselves why this information had not been applied in clinical practice;

and sometimes this is really basic information.

Slowly we became personally convinced that

patients would really benefit from many things

that are not discussed at medical conventions and read in textbooks

simply because they can reduce the consumption of pharmaceuticals

above all when this medicine are costly.

At a certain point we were convinced that Vitamin D

stimulated the production of quite a few neuroregenerative substances

in the brain of adults, children and embryos and fetuses. And it is extremely important,

as much for the development as for the function of the neurosystem (the same thing in the nervous system of an adult).

This knowledge is not available in medical texts

and the majority of doctors do not know the importance of this hormone,

which is not a vitamin but an hormone

that induces the formation of regenerative substances of the nervous system.

And we began, for this reason,

to administer Vitamin D to those that had neurodegenerative illnesses,

and became interested in Parkinson's patients

and began to give Vitamin D in physiologically realistic doses.

It is important to say that the daily dose that is recommended today, internationally,

doesn't include patients with Vitamin D deficiencies,

it's a paltry dose, much below the physiological dose.

And then we began to give the physiological dose, which is a dose of 10,000 daily units,

what one produces in just a few minutes of exposure to the sun.

Or, if you have a tank top and shorts on, with your legs and arms exposed,

what you will produce in 20 minutes. Or, if you have pale skin and are young, 10,000 units of Vitamin D will be produced every day.

So 10,000 is a physiological dose, not a super dose.

However most doctors consider this dose potentially toxic.

And these doctors maintain that today the recommended dose is 600 international units.

So, 600 international units are recommended

but if a person is exposed to the sun for just 20 minutes, it produces 10,000 units!

So there is an evident difference between medical practice and scientific knowledge.

So we begin to give 10,000 units to those with neurodegenerative illnesses,

and I remember a Parkinson's patient that received 10,000 of Vitamin D,

when the patient returned for the second visit, after 3 months (taking 10,000 IU every day)

the patient had a vitiligo lesion on his face

that had diminished a lot in just a few months of administering 10,000 IU.

This made us search for information in the medical literature

in relation to the effects of Vitamin D in the immune system.

We were surprised by the enormous quantity of publications that were already available in 2001-2002.

In line with this first result, we began to give 10,000 units of Vitamin D to patients

with multiple sclerosis, which is the most common autoimmune illness in neurology,

the one that has the most devastating effects of neurological patients.

We were surprised to see how much better these patients got.

This was the point of departure: the recognition of the great value of Vitamin D

in the treatment of autoimmune disorders.

Today we are absolutely convinced, together with the scientific community that pursues

research on Vitamin D, that studies the effects of Vitamin D in the immune system:

vitamin D is the largest regulator of activity in the immune system

and modifies the functioning of approximately 4,500 genes

in every cell of the immune system. It's a substance that has no peer.

I'll make a comparison

to explain what I mean with 4,500 genes that are regulated in their activity by vitamin D.

Imagine a skyscraper where there are many rooms. Imagine that

4,500 doors inside this skyscraper can be opened or closed by only one key.

So you need to compare the skyscraper with every cell of the immune system

and the key is vitamin D.

When there is a deficiency of vitamin D, the sick person can't regulate, in other words open or close,

stimulate or reduce the activity of 4,500 biological functions inside the cells of the immune system.

The deficiency of this substance amounts to a disaster for the immune system!

What does your protocol entail?

All the substances that constitute the treatment in reality are found in one element: vitamin D.

Those who have auto-immune disorders, according to what has been published in scientific literature

on the subject, have a partial resistance to the effects of vitamin D;

and this is genetically inherited from the father, the mother or both.

This resistance regards the immunomodulatory effects of vitamin D, and is a partial, not a complete, resistance.

This is the reason why these people are predisposed to develop autoimmune disorders.

The most important, maybe the only (perhaps the others are responsible for 5% of the results)

but 95% of the results that we obtained in the management of autoimmune disorders

in a particular way in the management of multiple sclerosis, the effects are due, in 95% of cases, to vitamin D.

We need to give very elevated doses of Vitamin D to get complete control of the illness.

These doses are not equal for all patients; they are specific to each patient

and are adjusted in line with the level of resistance that each person carrying the autoimmune disorder

has for vitamin D (to the level of resistance that the patient possesses in relation to the effects of vitamin D).

What we did was develop a method to adjust the daily individual doses for each patient,

which is done through lab tests.

The patient gathers lab tests before the treatment,

after which they take predefined doses of Vitamin D; two months

are necessary to increase and stabilize the level of Vitamin D in the patient's blood.

After two months the tests are re-done and and the results, before and after the treatment, are compared.

Through this comparison we are able to adjust the individual dose for a given patient

and two months after we have adjusted the doses we obtain

the complete effect, which means, in practice, suppressing the activity of the disorder.

The illness is suppressed after two months, after the adjustment of the daily dose.

How many patients have you treated with your protocol and what is the success rate?

Well, at the moment we are working with 5 doctors that are helping us here at the hospital. Personally, I've already seen about 1,300 patients.

At the clinic, if we consider the doctors who have been working with us for almost a year and a half, in all, 2500 patients have been seen

and we have also been training doctors who works abroad.

One of them, who is already working with our protocol,is in Argentina and others in several cities of Brazil.

These doctors have been receving hundreds of patients each.

So I can tell you that here at the clinic we have almost 2,500 patients who suffer from multiple sclerosis,

and we are referring to this pathology only. If we consider the other autoimmune diseases, we will

certainly talk of 3,000 patients, but as what concerns multiple sclerosis only, there are 2,500 patients.

This number can be even superior,

taking into account that we are not including in it those patients who have been seen

by 10 or 12 doctors working in other capitals of Brazil

after having made the medical treatment here.

Everyone must have seen more than one hundred patients,

so that this number has reached for sure thousands of patients seen

and, moreover, we have been receiving patients from different countries.

This is a phenomenon of nowadays connected with internet: people create groups

and this is in some way good, because patients can get in touch with one another

to compare the experiences they have had with the different treatments they have undergone.

This has created the phenomenon of today.

At present, most patients search for us after having entered the net.

We have a patient that you have also interviewed, whose name is Daniel Cunha and who is a journalist,

who reached a turning point ("high") in our clinic: he once had MS and this is a very important thing to say.

In fact, after we are able to adjust the treatment, that is the dose for the patient,

and we are able to prove that, in two consecutive MRI scans, the latter after one year, so separated one from the other by a pause of a year,

there's no new lesion, recent lesions have disappeared, and no other lesions activity exist,

so, when we can demonstrate this and the patient manifest some improvement,

if he has not older damages, he returns to have a normal life,

at the end of two years' treatment during which we schedule 3 or 4 medical examinations.

At the end of this period of two years of treatment, the patient reaches the "turning point":

it's necessary to maintain the dose of vitamin D with the preventative measures not to provoke intoxication,

but the dose of vitamin D has to be maintained and we recommend that the patient comes again after two years for a reevaluation,

then, after five years, for a new reevalution.

We still don' t know for how long the patient needs to maintain this high dose of vitamin D

and for the moment the treatment is for an indefinite period of time; asking to patients that they do this reevaluation

after two and five years, we may be able to establish, in this period of time,

a criterion to know if they can diminish the dose and who, among them, should continue instead;

but at the moment the treatment remain for an indefinite period of time.

What is the success rate of your protocol on multiple sclerosis?

Approximately in the 95% of patients with MS, the disease remains in permanent remission.

While they keep this high dose, the disease remains inactive,

with no signals, not even clinical nor of laboratory, of new lesions.

A 5% of patients obtain a partial result; it means that they have improvements

but they don' t have the complete remission of the disease activity.

We are studying the reasons for which this 5% can' t reach

the complete remission of MS and we have arrived to define two main points:

the most important is a level of stress extremely high.

Now we know that emotional stress can seriously affect the result of this treatment.

The other element that can compromise the success of this therapy is the habit of smoking:

tobacco addiction limits the success of treatment with vitamin D,

but this is not an element to be specifically related with the issue of vitamin D;

actually there are many data in medical literature explaining that the smoking habit accelerate the development of MS,

even if the patient is under traditional treatment.

When I talk of 95%, I mean those patients who did no other type of treatment if not a high dose of D vitamin,

associated with a diet and abundant hydration, which are necessary to avoid side effects.

Apart from that, it may be that recurrent infections such as urinary tract infection

in those patients that before starting this treatment already suffered from a series

of problems connected with bladder and urinary function,

who have so an enhanced susceptibility to recurrent urinary infections:

we know that these recurrant urinary infections can reduce the immunomodulatory effects of vitamin D.

I speak of immunomodulatory effects because vitamin D doesn't suppress the activity of the immune system.

At present we know that vitamin D suppresses specifically the type of immunological reaction,

not physiological, that is known with the acronym "TH17",

which is the immunological reaction that provokes autoimmune diseases.

Thus, all autoimmune diseases, that is to say this aggression of the immune system against its own body,

are caused by a type of reaction that is not normal, not physiological, it's aberrant and it s called "TH17".

Vitamin D is the only substance, for what I know,

is able to selectively inhibit this reaction, without undermining the other reactions of the immune system.

More than this, vitamin D strenghtens the capacity of the immune system to react against viruses, bacteria, like the Tb bacillus.

The ability of our immune system to react against these micro-organisms

is strenghtens by the supply of vitamin D.

It' s already well-known in the scientific community that those who have tubercolosis need

a supply of vitamin D so that the anti-tubercolosis effects can be more effective.

Moreover, it' s well-known also that the HIV carriers patients, for instance, or hepatitis C virus carriers too, they both need to be supplemented with

strong doses, and not with daily doses internationally "recommended",

but, on the contrary, of a phisiological amount of 10.000 units a day, so that hepatitis C virus doesn't cause too many damages in the liver,

as it would be if there was a deficiency of vitamin D.

The same thing happens for the other examples of HIV and tubercolosis.

What is the success rate on inflammatory bowel diseases such as ulcerative colitis and Crohn's disease?

At the same time, Chron's disease, inflammatory intestinal diseases including ulcerative colitis,

are diseases over which we have managed to have complete control using the same protocol of treatment.

It's important your question, because the use of vitamin D in the treatment of autoimmune disorders

is not aimed to a specific disease but to regulate the immune system. For example:

under the effect of Vitamin D, the immune system increases the quantity of a type of cells

which are produced by the immune system with the purpose of maintaining it regulated.

These are called "regulatory T lymphocites" and the quantity of these cells increases very much under the effect of vitamin D.

In the same way, the Th17 reaction, that is abnormal, not physiological,

aberrant, is selectively inhibit by vitamin D.

Both these things are extremely important for the control of any autoimmune disorder.

These autoimmune diseases that you have mentioned as intestinal inflammations, Chron's disease and ulceral colitis,

are cases that we have treated and which have responded completely.

The patient lives utterly free from any manifestation and symptoms of the ilness and leads a daily normal life,

but he also has to continue the diet about which I've talked before. He can't eat dairy products,

and no food made of milk and he also has to keep an hydration of at least 2,5 liters of water a day.

I repeat it: the autoimmune diseases that you have mentioned, up to now all the cases,

which are not so many as the cases of multiple sclerosis, but are nevertheless dozens of cases,

they have all responded in a complete way without suffering the side effects of vitamin D at elevated doses.

Why haven't you worked yet on a double-blind trial on your protocol?

This question is very important because we can't randomise metabolic mistakes.

I mean that, if there's one person who has a metabolic disorder diagnosed through laboratory...

for example a person with hypothyroidism: deficiency in thyroid hormones,

that is potentially lethal and can cause damages to someone's health if it is not adjusted.

Another example is that of type 1 diabetes, in children that can't produce insuline,

I'm obliged to correct this deficit and I need to administer them insuline.

So, on those circumstances, when the patient has a metabolic problem,a deficiency,

a sort of resistance inherited, in relation to a hormone or a vitamin, I' m obliged to intervene to adjust it.

If I don't correct it, I will make a mistake of therapeutic negligence.

So, if u are talking of a double-blind and randomised research, you are saying to me

that I have to keep one group of patients that will be treated for example with high doses of vitamin D

and a group of patients who will receive a placebo;

and both doctors and patients involved in this research don't know

which patients are receiving vitamin D and which are reiciving the placebo.

Very well, I couldn't do this kind of researches with diabetic children, for example.

We have never done a randomized double-blind research to know

if insuline is suitable for diabetic children. We have never done and will never do.

The same happens with people with hyperthyroidism, since we are forced to give a treatment.

A randomized double-blind study will never be done, where a group will receive the thyroid hormon and the other a placebo.

The same happens in case of a deficiency of vitamin D.

A vitamin D deficiency can cause a devastating neurologic disease destroying the spinal cord,

so you can't leave a person that suffers from a deficiency of vitamin B12 without treatment, because I would be negligent.

You can't leave a person that suffers of pellagra, with a deficiency of niacin (vitamin B3) without treatment, because this can cause diarrhea,

dermatitis and even death. So, you can't leave these persons with a deficiency.

if I make a randomized double-blind study, I will be negligent with 50% of my patients.

The placebo group will be victim of medical negligence.

This is a very important concept

because nowadays medical class is said that all the results published in the literature

are not to be considered if they aren't the result of a randomized double-blind study

This is a big mistake.

People with a vitamin D deficiency or resistance to the biological effects of vitamin D,

in their case this deficiency has to be corrected and resistance compensated with higher doses,

that could restore, in this person, all the biological effect of vitamin D.

Then, we don't have any randomized double-blind study and we will never do with any patient

because two great basic principles in the medical activity exist, that are teached in all western medical schools around the world.

The first principle says not to worsen the state, not to hurt

not to act on your patient in such a way that worsens his clinical state.

And the second principle says that the patient has to receive all the possible benefits.

Then, if I left a patient with a vitamin D deficiency

aware that the vitamin D is a great immunomodulator, perhaps the most powerful immunomodulator substance existing in nature,

a patient with an autoimmune disease and has an unregulated immune system

and produces an aberrant immunological reaction, not physiological, called TH17,

if I left this patient with a deficiency of the only substance that, selectively, in a powerful way

is able to inhibit this TH17 reaction, producing normal linphocites, I will be negligent toward this person

Then, I will never do a randomized double-blind study using vitamin D and placebo

with persons having autoimmune disease. Why? Because I would't do this sort of things with my daughter,

my wife and even my patients.

Is there any observational study (not double-blind or similar) issued or pending, about your protocol? If not, why?

We started using vitamin D to treat autoimmune disease for the patient sake

Our objective wasn't the research, wasn't to convince anyone

but was simply satisfying the second principle of the medical practice:

to benefit the patient in the most optimal way

namely, if the patient has a deficiency of a powerful immunoregulator, known and documented,

we have to correct this deficiency.

If he has a resistance, we have to increase the dose in such a way that this deficiency is compensated

Then, we have gathered much data during this period, and we got experience about the adjusting of the dose for these patients.

We have published many preliminar data about vitiligo and psoriasis, and these are the only diseases which we were able

to make approved by the ethical-medical committee of the UNIFESP (our university) the research for.

We would like it done also for other diseases, but, unfortunately, factors exist, that many times we don't understand

because are againt the willingness to do a treatment that could benefit,

in the same way we don't understand how the ethical condition to correct a deficiency in a patient could be denied.

I am not able to understand, however the answer has been negative for some kind of diseases.

This hasn't stopped us from continuing to treat our patient according to their interest

and we have accumulated a great experience of very well documented cases.

And when we will have the possibility, we will solicit an ethical committee that allowed us to evaluate retrospectively these cases

if this will be possible. Because we have rules for scientific publications.

Then, when I will submit a publication to a magazine where there are 2,500 patients treated with high doses of vitamin D

and we will like to publish the outcome of cases, the magazine editor will ask us where is the approval of the ethical committee

otherwise we will not able to publish this our experience.

Then, first we have to solicit the ethical committee

so it approves a revision of the medical records of these patients.

With the revision of the medical records we could send the material to the medical magazine. Let's hope not to have problems

as to the retrospectively revision of the medical records of the patients during the 11 years of monitoring

However we don't know why sometimes certain people takes inadequate decisions

about the disclosure of the knowledge and the patients sake.

Is the success rate the same as that of Multiple Sclerosis even with patients suffering from psoriasis?

Yes, just like that, the percentage of success is similar to multiple sclerosis.

But it is important to say that when we published these works about psoriasis and vitiligo,

we used a fixed dose for all patients of 35,000 units a day

associated to a diet without dairy product, to avoid toxic effects to the kidneys, and abundant hydratation.

On that occasion we didn't use this method of individual adjustment of the dose for each patient.

We got these results in the 95% of patients, when we used this method

of individual adjustment of the dose for each patient,

taking into account the laboratory response that each patient shows,

through the comparison of the laboratory tests, done before and after the treatment, namely after 2 months.

Then the result, in other words, has reached the 95% of success

when we started using this adjustment method,

based upon the response of the individual laboratory tests

that every patient shows to a common preestablished dose.

For what kind of neurological diseases is your protocol suitable and why does it work?

Then, high doses of vitamin D generally work in case of autoimmune diseases.

The neurologic autoimmune diseases where we used vitamin D,

besides the multiple sclerosis, are: isolated optic neuritics,

the Gullame Barre syndrome (GBS), the autoimmune polyneuropathy,

the severe myastenia. These are the autoimmune neurologic diseases I remember now.

The result of this treatment, when we use the method of individual adjusting of the doses

for each patient, was the same of the multiple sclerosis: 95% of complete suppression of the autoimmune activity.

That doesn't mean that the older irreversible damages caused by the immune system,

considering as preexisting damages, regress.

Generally, we obtain as result a complete or almost complete, regress of the damages

formed 1 year before the beginning of the treatment with high doses of vitamin D.

Besides skeletal and autoimmune diseases, in which other case may your protocol be useful?

There are other diseases, whose outbreak is favoured or is dependant

upon vitamin D deficiency.

For example, the repeated abortions in the first quarter of pregnancy.

Till today, this is considered an autoimmune disease.

The autoimmune system refuses the embryo implantation.

This events depends upon a vitamin D deficiency

and a partial resistance to the biological immunoregulator effects of the vitamin D.

Also the presence of hypertension, high or very high blood pressure, at the end of pregnancy,

in the so called situation of "eclampsia or pre-eclampsia", putting at risk the life of the mother in the final phase of pregnancy,

for which the obstretician must anticipate the birth with a caesarean section.

All that can be avoided administering suitable doses of vitamin D.

As suitable doses I mean 10,000 daily units.

Besides, pregnat women, that don't enough expose themselves to the sun,

so favouring very low levels of vitamin D, run a high risk to give birth

to children that, later, could develop an autism problem.

Autism is higly favoured by the deficiency of vitamin D during the pregnancy and during the first years of life.

The deficiency of vitamin D, that appears at the beginning of the life of a person or during the end of pregnancy

or in the first years of life, much increases the possibiity that this person, when he will reach the adolescence

develops psichiatric diseases as, for example, schizophrenia.

Regardless of the age, the deficiency of vitamin D much favours the appearing of depression.

Depression processes are favoured or induced by the deficiency of vitamin D,

that is seldom taken in account by doctors that are nowadays treating people affected by depression.

It is important to talk about diabetes.

Either the type 1, that is autoimmune, or the type 2, that is that one of the maturity,

either ones are higly favoured by the deficiency of vitamin D.

The insuline production is favoured by the vitamin D.

The vitamin D deficiency favours the developing of diabetes.

As to diabetes, the effects of the vitamin D deficiency are subject of several researches.

These diseases are the most important to be mentioned as to their relation to the vitamin D.

Does your protocol also improve the ability to excrete heavy metals in patients with MS, since they have an enzyme deficiency?

I have no information about that, but it doesn't mean it doesn't exist,

if the vitamin D could favour the elimination of heavy metals from the body, I don't have this information.

I am strongly convinced that the outbreak of autoimmune diseases mainly depends upon three factors:

we consider a person that has inherited this predisposition from father or mother,

or it concerns a partial resistance to the biological effects of the vitamin D.

It depends upon a second factor that is the vitamin D deficiency, caused by a poor exposure to the sun.

And the third factor is the emotional factor.

This last one would be the triggering factor which leads to the activation of autoimmune deceases,

including multiple sclerosis,

in people having the other two predisposing factors to developing this diseases.

What's missing is the triggering emotional factor

such as a highly stressful life event. For example:

a teen boy or girl involved in their parents' separation;

a 18, 19, 20 years old individual experiencing an emotional break;

a 30-35 years old person watching his or her marriage breaking up;

an adult person coping with his or her child's unexpected death.

In the end, these emotional traumas lead to relapse of autoimmune diseases, multiple sclerosis included.

Since for 95% of our patients the disease is brought under total control at present,

by using high dose of vitamin D.

We are not excluding other factors that may also play a role in the process,

anyway even if these factors may actually be contributing to the development of autoimmune diseases,

the role they play is a minor one compared to the physiopathological importance of vitamin D

or to the lack of immunomodulatory biological effects of vitamin D in our organism.

Is it vitamin D deficiency that causes autoimmunity and inflammation or is it the pathological state itself to rather cause vitamin D deficiency?

Many researchers assume that persons with multiple sclerosis,

because of the neurological deficiency that hinders them from walking freely,

tend to stay indoors, inside the house,

that is why they get less exposure to the sun thus resulting in a lack of vitamin D.

Therefore they affirm that vitamin D deficiency is a consequence of the disease and not the cause of it.

So that would be the matter.

Well, that is not explaining why, and there have already been studies published in 1986,

when evaluating a patient, over the years, the relapse rate,

before and after being treated with vitamin D,

a drastic reduction of relapse rate occur after treatment. The relapse rate decreased drastically.

This kind of reasoning is excluding the fundamental and well-documented role of vitamin D as an immunomodulator.

In plain words, vitamin D inhibits reactions in every autoimmune disease

including the non-physiological aberrant reaction, called TH17.

Vitamin D increases the number of immunomodulatory lymphocytes.

The more the vitamin D level, the less the autoimmune activity of the disease; the lesser the vitamin D level is, the highest the autoimmune activity of the disease will be.

If you consider all these factors together, there is just one explanation:

the lack of vitamin D leads to autoimmune diseases.

Another factor to possibly consider, in order to explain how the lack of vitamin D

plays a crucial or an additional role in the manifestation of autoimmune diseases,

is the one related to the distance from the equator line.

Since the farther you move from the equator line, the more autoimmune disease cases occur.

If you analyze a Country distant enough from the equator line, as Norway, for example,

you will find that in northern Norway multiple sclerosis level,

in contrast with the rule of the equator line, you will find less cases of autoimmune diseases such as multiple sclerosis,

if compared to southern Norway, where the city of Oslo is located.

This is also explained by the role vitamin D plays,

since in northern Norway diet is basically made of cold water fish consumption.

These are high-fat fishes, such as sardines or salmon, whose fats contain large amounts of vitamin D.

Therefore we may invert the equator rule when vitamin D is available.

And it's the same in Switzerland, on the swiss Alps, in those places located at about 2,000 meters of altitude.

Vitamin D blood level in people is higher then in northern Switzerland

and northern Switzerland is closer to the sea level. So, why is this occurring?

We can explain it by sun exposure.

In districts located at high altitudes, above the clouds, you get much sun.

Autoimmune diseases are not fostered by frigid temperatures,

because, on the contrary, in the swiss Alps they would have more cases.

In the swiss Alps there are less cases because of the greater exposure to the sun and consequently more vitamin D.

In northern Switzerland there is less exposure to the sun

thus resulting in lesser amounts of circulating vitamin D in the blood of inhabitants of high mountain climates and consequently more autoimmune diseases.

Every epidemiology regarding autoimmune diseases is made comprehensible by a unique factor:

the lack of vitamin D.

You may get to consider a unique factor,

just one characteristic of vitamin D epidemiological distribution and say: "No, anyway there is an alternative explanation,

people affected by multiple sclerosis, patients with a more severe form of multiple sclerosis,

have a major vitamin D deficiency because they stay more at home."

This is an alternative explanation even though it does not answer more enquiring questions about vitamin D biological functions,

about all the other epidemiological characteristics of vitamin D. Epidemiological characteristics of autoimmune diseases.

Do you agree whit the affirmation that measuring the parathyroid hormone is critical, since it's a kind of litmus test used to verify the metabolism of vitamin D?

Parathormone (PTH) level is extremely important for us.

Why? Because when you administer vitamin D, vitamin D inhibits parathormone production.

Therefore if I measure hormone levels before starting administering vitamin D and then after two months,

I'll succeed in using the parathormone level reduction (i.e. how much PTH decreased by administering vitamin D)

as an indicator of the biological answer to vitamin D effects.

This is exactly the parameter we use to individually adjust vitamin D dose.

If vitamin D inhibits PTH production,

I'll raise vitamin D level until the PTH value is decreased under the normal limit.

I do not suppress PTH, i just raise vitamin D until PTH approaches the lower limit

within the normal of variation for PTH.

Because of this biological effect I deduce that if vitamin D obtains the maximum effect in the inhibition of PTH,

it must have reached the maximum immunoregulatory effect as well.

So, through this premise, we adjust vitamin D intake according to the decrease in serum levels of PTH.

I can't suppress PTH causing it to be undetectable because if I did that

the patient's life would be at risk.

The patient is taking such a high dose of vitamin D that a large amount of calcium could be drawn from bones.

Raising this excessive amount of calcium, drawn from bones, and increasing its blood concentration, it may be possible to compromise renal function.

Thus, parathormone is a safety parameter for us, a security level.

If I do not suppress parathormone, I'm sure I'm not giving toxic doses of vitamin D.

I can balance it in according to the specific biological resistance to the effects of vitamin D that the individual has for hereditary genetic reasons.

Let me put it in other words.

An individual may need a specific dose of vitamin D, for example 30.000UI,

so that PTH level may reach the lower limit of normal range.

Another individual may need 100.000 UI so that PTH may reach the inferior zone of the normal range.

Then by measuring the decrease of PTH we adjust vitamin D doses,

depending on the individual need of the patients.

PTH level is the easiest lab test available,

which gives us the idea of the person's resistance to the effects of vitamin D.

Other possibilities exist, other parameters to be eventually measured.

Anyway a test to measure the amount of PTH can be done by any laboratory, I mean it's nothing exceptional.

Many physicians request a parathormone blood test.

So, this is not an exceptional test, it is an easily available test in any laboratory around the world.

What should be the ideal level of 25(OH)D3 and PTH in a person suffering from an autoimmune disease, and what in healthy people?

I've somehow answered this question already.

A person showing a PTH level close to the upper normal limit,

is more likely to have an important deficiency of vitamin D.

And it is drawing calcium from bones so as to maintain blood calcium concentration,

since there is not enough vitamin D to absorb calcium from intestine,

from the food passing through intestine and digested in the intestine due to of vitamin D.

So, a person whose parathormone level is close to the upper limit of normal range

or beyond normal upper limit, has a very severe vitamin D deficiency.

And this is something that varies from person to person, including those affected by an autoimmune disease

as well as a healthy individual.

For example, the fact that a person is not suffering from an autoimmune disease today,

doesn't mean that won't get an autoimmune disease at any moment of life.

So, in terms of prevention,

it is of the utmost importance that a person maintain PTH level at least at the mid-range point,

between the lower and the upper limits within the normal range of values, through a realistic administration of vitamin D.

Then, the same healthy individual, taking vitamin D, 10,000 IU,

probably (not definitely, but probably) this dose will be sufficient to keep

his parathyroid hormone within the normal range of variation.

Neither close to or above the upper limit.

What is the ideal level of parathyroid hormone in the blood?

Yes, this is an important thing...

Laboratories have different ranges of variation (range) to assess the normality of the parathyroid hormone.

Then, a laboratory can affirm that according to their test procedure, the way they measure the parathyroid hormone,

the normal level varies, for example, in the range of 4 and 58 pg/mL.

Another laboratory can say that for them the normal range is 12 to 65 pg/mL.

So, the question concerning a level which is below 20

is for people who use a lab where the normal range of assessment is 12 to 65.

Then it must be between 20 and 12.

But with a person who uses a further laboratory where the normal range is 4 to 58,

then I must remain between 10 and 4.

The same thing I've explained before.

I must be close to the lower normal limit, but not below the lower normal limit.

I dose vitamin D to achieve this effect.

So, it's not necessary to be below 20.

Below 20, or below 10, or between 12 and 20 or between 10 and 4, it depends on what is the normal range

that the laboratory uses as a reference.

So, it depends on the laboratory.

What should be the best supplementation for vitamin D? Daily, weekly, monthly or yearly? And why?

We have not yet assessed whether a weekly administration may be better or worse

than a daily dose, or if a monthly administration may be better or worse

than a weekly administration.

We haven't done studies about it.

We have just started from the assumption that a daily sun exposure is a good rule for people to follow.

So, if this is the norm, we try to adjust the dose according to daily administrations,

and this is justified by the fact that we avoid the big variations

caused by administrations far between one another.

So, when we administer on a daily basis,

the variation of blood concentration keeps more regular, less unstable,

and the range of variation will be minor.

Those who follow the protocol should drink at least 2.5 liters of water. What about healthy people who take only 10,000 IU per day?

Who takes 10,000 units per day is taking a physiological dose,

the same amount that his skin would produce when exposed to the sun for twenty minutes, without sunscreen,

wearing a short-sleeved shirt and shorts,

in other words leaving his arms and legs exposed to the sun, being a person of fair skin and young.

So, this can't do any harm to anyone because it is the amount that we normally produce.

So, it's not necessary to go on a diet or any special hydration,

besides what each individual should normally do to stay healthy.

There is no need to take any precautions when taking 10,000 IU of vitamin D.

My daughter has been taking 10,000 units of vitamin D per day for more than six years.

There is no problem in taking 10,000 units of vitamin D per day,

there is no need to take any precautionary measure.

This, for sure, is not a toxic dose,

this dose is sold without a medical prescription in the United States without any problem.

How does your protocol interact with the intestinal microbiota, the digestive system and the VDR (vitamin D receptors)?

So, we do not really know of any effect of vitamin D on the normal gut flora. Whether there is a publication in this regard, then it is not to my knowledge.

Since Vitamin D increases the power of reaction against pathological agents,

we can also expect Vitamin D to reduce the presence of harmful bacteria in the gut. We hope that.

I have no information saying that vitamin D may harmfully alter the digestive system.

It is possible that a lack, a deficiency of vitamin D is likely to affect the work of the digestive system,

since all our cells, including those of the digestive system, biologically respond to the effects of vitamin D.

It alters its functions in relation to the effects of vitamin D.

The own activity of the digestive system may be favored by the correction of vitamin D deficiency.

However, harmful effects caused by high doses of vitamin D (unless they are toxic, that is accompanied by a corresponding increase of calcium in the blood),

there can't be harmful effects to the digestive system, using high doses of vitamin D, calculated according to the laboratory tests.

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...

What is the relationship between vitamin D and phosphorus?

We have measured phosphorus because vitamin D mobilizes both calcium and phosphorus from the bone tissue.

And since we are using unprecedented doses of vitamin D, this was also suggested

by Professor Michael Holick, so we have to document everything that is going on.

One of our concerns is phosphorus not being altered;

phosphorus levels not being altered.

In fact, the dose we use, together with these precautions, do not alter the levels of phosphorus.

It's merely a precaution

to be sure that patients are doing well from a laboratorial point of view.

All the laboratory parameters that can be altered by the use of high doses of vitamin D are measured

and this is just one of them.

That's the reason why we measure the levels of phosphorus.

What is the role played by vitamin D in clinical renal failure?

Patients with renal failure, it is a big problem for us

to give them high doses of vitamin D.

Because if I administer a dose of vitamin D causing an excessive calcium absorption, both in the bones and in the gut,

I must be sure that the kidneys will excrete it;

however, if a person suffers from kidney failure, I lose this certainty.

So, if a person has a kidney failure, this causes much more work,

we must be much more careful with him/her than with a person who has normal renal function.

This is the only thing I can say about kidney failure.

There are diseases such as systemic lupus erythematosus, where the immune system attacks the kidneys.

We try to "stop" lupus before it causes kidney injury.

If a person already shows kidney injuries we must be much more careful.

We start with a low dose of vitamin D to be sure that nothing will happen to the person.

There is a need for the kidneys to expel the excess calcium that is formed in the circulation

and if the person has a kidney failure this becomes a problem.

Is the integration of vitamin D incompatible with G6PD deficiency (favism)?

G6PD deficiency is one of the diseases that have increased in Italy in consequence of endemic malaria.

People with G6PD deficiency are resistant to malaria.

It is the same type of natural selection that has happened with the deficiency of riboflavin.

But I have no data showing that vitamin D and G6PD deficiency are incompatible things,

in the sense, that I can't give vitamin D to people who have glucose-6-phosphate dehydrogenase deficiency,

which is called G6PD.

I see no incompatibility.

What is the relationship between vitamin D and dystonia?

I do not have this information, that vitamin D may help people with dystonia.

For now I do not have it, but I can do a search,

since vitamin D is a substance having a lot of functions,

all cells respond to vitamin D;

the fact that I have no information about this, or the fact that no study has been published on the relationship between vitamin D and dystonia,

these things don't indicate that vitamin D may not be beneficial to people with dystonia.

But I really do not have an available information at this time.

Have you ever had patients with ALD (adrenoleukodystrophy)? Is it possible to treat it with your protocol?

No, we have no patient with adrenoleukodystrophy, which is a metabolic disorder.

There is no direct relationship with vitamin D.

Many people who have degenerative diseases of the nervous system, can potentially be facilitated

by a reasonable dosage of vitamin D.

Surely, these people cannot remain with a vitamin D deficiency, or two factors would overlap:

a genetic, hereditary and metabolic disorder, typical of that disease and, in addition, a vitamin D deficiency,

which can accelerate the progression of the disease.

So, we suggest to people who have neurological or metabolic diseases that do not have a direct relationship with vitamin D,

we suggest that they should, more than other people, maintain normal levels of vitamin D.

We do not recommend high doses of vitamin D, but only normal doses of 10,000 IU per day.

These people should care, more than others, about being not deficient in vitamin D.

Can a patient take vitamin D and Coumadin at the same time?

For a patient who takes these anticoagulants with vitamin D?

Basically there is no incompatibility with vitamin D, with the treatment with vitamin D,

or with high dosages of vitamin D, always observing precautions: diet and hydration.

We have no information that it would cause any problems with the use of anticoagulants.

An important warning is for people suffering from hyperthyroidism, or high levels of thyroid hormones,

and who do not take drugs or do not follow a treatment that maintains normal levels of thyroid hormones,

these people can be very sensitive to the toxic effects of vitamin D.

The thyroid hormone increases the effect of vitamin D in mobilizing calcium from the bones.

Those people are more sensitive to vitamin D, those with untreated, uncontrolled hyperthyroidism.

This is a warning, we have already had two cases of people who have developed hyperthyroidism,

who have become more sensitive to vitamin D than what usually happens;

the sensitivity level of these people is higher than that of people having a normal thyroid function.

Is there any medication incompatible with vitamin D?

Yes, we say to patients who need to take antibiotics or anti-inflammatory drugs that are toxic to the kidneys,

that they must increase hydration. It's not enough drinking 2.5 liters of fluid,

but a liter more: 3.5 liters of fluid per day,

because when the drug passes through the kidneys, in this way it is diluted and the nephrotoxic effect, that is toxic to the kidneys, decreases.

Do you think that it is necessary to be under medical supervision to take 10,000 IU per day?

The person who takes 10,000 units of vitamin D is taking the same amount of vitamin D

that a young man would produce in his skin when dressed in short-sleeved shirt and shorts,

leaving his arms and legs exposed to the sun, a young person with fair complexion, without the use of sunscreen,

would produce 10,000 IU of vitamin D, which cannot be considered a toxic dose of vitamin D.

And there's no need to do laboratory tests or to be under medical supervision,

for the simple fact that an adult is taking 10,000 units of vitamin D.

This, however, is not valid when it comes to children;

this dose may be excessive for underweight children.

Are you willing to come to Italy for a symposium on your protocol with high doses of vitamin D?

Yes, but it's important that the symposium has a logic and that it is productive;

that it can allow to get in touch with professionals willing to work with this protocol,

using vitamin D on behalf of the patients, in this case we are interested.

It would be less productive to go to Italy to just do what we're doing here right now,

that's to say to just orient the public, since we would only be repeating the same things.

The medical staff and other professionals who are interested in the results of this treatment,

may ask technical questions that have not been discussed here today.

So, in this case a trip to Italy would be very productive,

for the amount of people that could have a benefit with this treatment,

for young people who may become blind or paraplegic due to multiple sclerosis,

or who might suffer for a lifetime the effects of a disease such as inflammation of the colon, and many others already mentioned.

The presence in Italy of a professional who puts into practice this treatment,

would provide an immeasurable benefit to people who live in Italy.

One has no idea of the benefits that one might have.

And he would have the same satisfaction, the same level of gratitude, immense, that we are receiving,

keeping people away from the relapse ("alta") of multiple sclerosis and autoimmune diseases.

We lose a patient when it reaches the expected result ("alta"),

but as a reward we receive a friend for life and this is something priceless.

There are 2.5 million people worldwide suffering from Multiple Sclerosis only.

Tens of millions have instead a diagnosis of autoimmune disease.

How many of them have their level of vitamin D and parathyroid hormone measured?

Prior to be prescribed a medication, ask your doctor to check these parameters. Your health is at stake!

Physicians interested in knowing the Coimbra protocol can write to: cgc.secretaria@gmail.com
Subject: "ESTAGIO DE MÉDICOS ITALIANOS - L. RUBINI"

THANKS TO:
Mona Motiramani, Iara Pavoni, Juliana Lopes Marinho, Christian Porcaro, Matteo Gennari, Isabel Cristina Guandalini Cilla, Juliana Lopez Marinho, Enri Tommasin, Alessandro Tuoni, Caterina Brunelli, Andrea Ceravolo, Matilde Costantini, Jonathan Mullins, Nicola Pace, Chiara Schenetti and Simonetta Silvestri.

Luisa Rovati

This is a non-profit action because health is priceless, as well as the gratitude of people.
www.leonardorubini.org
 

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burtlancast

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Is the bit D given orally by liquid?

Any suggestion of best brands? @burtlancast

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.
 

burtlancast

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Here's the most interesting part of the interview:

Vitamin D doesn't suppress the activity of the immune system.

At present we know that vitamin D suppresses specifically the type of immunological reaction that is known with the acronym "TH17" which is the immunological reaction that provokes autoimmune diseases.

Thus, all autoimmune diseases are caused by a type of reaction that is not normal, not physiological, it's aberrant and it's called "TH17".

Vitamin D is the only substance, for what I know, able to selectively inhibit this reaction, without undermining the other reactions of the immune system.

It does so by substantially increasing the quantity of "regulatory T lymphocytes" whose purpose is to maintain regulation of the immune system.

More than this, vitamin D strengthens the capacity of the immune system to react against viruses, bacteria, like the Tb bacillus.

The ability of our immune system to react against these micro-organisms is strengthened by the supply of vitamin D.

It' s already well-known in the scientific community that those who have tuberculosis need a supply of vitamin D so that the anti-tuberculosis effects can be more effective.

Moreover, it' s well-known also that the HIV carriers patients, for instance, or hepatitis C virus carriers too, they both need to be supplemented with strong doses, and not with daily doses internationally "recommended", but, on the contrary, of a physiological amount of 10.000 units a day, so that hepatitis C virus doesn't cause too many damages in the liver, as it
would be if there was a deficiency of vitamin D.

The same thing happens for the other examples of HIV and tuberculosis.
 

GAF

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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...
 

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."
 

Amazoniac

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Messages
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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."​
 

Perceiver

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Joined
Aug 27, 2019
Messages
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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?
 

Amazoniac

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Not Uganda

Amazoniac

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Joined
Sep 10, 2014
Messages
8,583
Location
Not Uganda

"Dietary calcium level and 1,25-(OH)2D3 are critically linked in the prevention of EAE in mice. When mice are fed a diet containing high calcium (approaching commercial diets), 1,25-(OH)2D3 at appropriate doses is 100% effective in preventing EAE. In contrast, when calcium is removed from the diet, 1,25-(OH)2D3 is only 50% effective in preventing EAE. When an intermediary level of calcium is fed, the effectiveness of 1,25-(OH)2D3 is intermediate between a low calcium and a high calcium diet.

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"Th-1 cells are believed to cause EAE. This belief is strongly supported by the finding that transferring a Th-1 cell clone specific for MBP to naive mice results in EAE (Powell et al. 1990). Therefore, our results strongly support the involvement of calcium in the action of 1,25-(OH)2D3 for the regulation of this T-helper cell–dependent autoimmune disease (Holda and Swanborg 1982, Powell et al. 1990)."

"It is of some interest that in mice fed a low calcium diet, doses of 1,25-(OH)2D3 that nevertheless produce frank hypercalcemia produce little or no further reduction in the incidence of EAE. Thus, in the absence of a dietary source of calcium, 1,25-(OH)2D3-mediated increases in serum calcium are ineffective for the further suppression of EAE. On the other hand, there are doses of 1,25-(OH)2D3 that do not cause hypercalcemia but that nevertheless reduce the incidence of EAE. Overall, our results argue that the 1,25-(OH)2D3 may function by both calcium-dependent and calcium-independent mechanisms to suppress EAE."



- Vitamin D Really Toxic?


"Others supplements are used to empower the results of Vitamin D in your system. Increasing the good effects in your brain and immune system.

A specific Complex of Vitamins & Minerals - in each pill has:

- Zinc: 5 milligrams
- Choline 120 milligrams
- Magnesium chloride or glycinate: 125-250 milligrams
- Riboflavin: 50-100 mg milligrams
- Vitamin B12: 1,000-5,000 micrograms
- Folic Acid: 500 micrograms
- Chromium Picolinate: 150 micrograms
- Selenium: 50-100 micrograms

- DHA: 500 milligrams (although this can vary depending on the patient's case)

The patient must take 4 pills per day. Or 1 pill every six hours.

- CoQ10 : 100mg 1x/daily (optional)"



Where's Belize? He disappeared.
 

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