Tto. del SFC como inmunológico, usando inmunoestimuladores

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elipoarch
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Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por elipoarch » 18 May 2012, 20:16


Otra muestra a favor de la teoría autoinmune del SFC :thumbup:
Se trata de una transcripción del siguiente video del Congreso sobre autoinmunidad de Granada Mayo 2012.:
[youtube]http://www.youtube.com/watch?v=2IMdAV6SIMU[/youtube]


Os pego la transcripción aquí por si queréis usar la traducción automática.

[t]Treatment of Chronic Fatigue Syndrome as an immunological disorder, using a novel immunostimulatory therapy[/t]
INGE LINDSETH - Clinical Nutritionist, 4M-klinikken, Norway
Autoimmunity Research Foundation, CA, USA


Transcript

00:00:08
I am a clinical nutritionist working at a multidisciplinary clinic in Oslo. Over the last decade my clinic and several other clinics around the world have treated various chronic diseases with a novel immunostimulatory therapy, also known as the Marshall Protocol.

00:00:30
Results of this therapy have been presented at various Autoimmunity Congresses the last few years, the last time in Singapore by Doctor Goetze-Pelka, where she pointed at the inflammatory nature of psychiatric diseases and pointing to the possible etiological role of persistent, chronic infection.
While CFS, which I am going to talk about today, is not regarded as psychiatric disease, the cognitive dysfunction can be severe, adding further weight to the close connection between the body and the brain in chronic disease. Thus, our approach, whether the symptoms stem mostly from the brain or the rest of the body, is to treat the disease on a whole body level.
In my talk I am going to talk about the basis for our treatment approach and tell you about you the results we are seeing in our CFS patients.

00:01:26
Before we get to that, I just want to point out the poor prognosis CFS patients generally have. In the cohort represented here, at the start of the observation period, the subjects had a physical function at about 40 on the SF-36 Physical Function scale. This is a level of functioning which implies only being able to take care of little more than one's most basic needs, and not being able to work, for instance.

00:02:03
So, over 30 months, you see there is little improvement, although there are individual differences in the trajectories, and as the author says, he doesn't recall any complete remissions in this cohort and nobody returned to work.
So, new solutions in terms of treatment are clearly needed in this disease.

00:02:11
We use an immunostimulatory therapy in this disease. Why would we want to do that?
Well, there are several lines of evidence pointing at infection being the cause of CFS.

00:02:31
One line of evidence comes from the fact that there have been several epidemic type outbreaks of CFS, and when a disease spreads in an epidemic manner, one of the usual prime suspects are infections.
As you see in the Norwegian Giardia-induced Bergen outbreak (2004), an actual infectious trigger has been identified as the cause.

00:02:59
Another line of evidence comes from the fact that most CFS patients experience flu-like symptoms at the start of their disease, as exemplified here in this large Norwegian cohort.

00:03:12
And although the findings are mixed, autoantibodies have also been found in CFS to be increased compared to control group in this study.

00:03:25
Also, findings of increased levels of IgM and IgA against common enterobacteria have also been found. I would like to also add that the level of symptoms that the patients have is correlated to the amount of IgA and IgM in these patients.
So, you have all these infectious associations and many more that I have not mentioned here today, but when it comes to finding one single living microbe—one single species of microbe—in this disease, the results are scarce and mixed.
This could mean that infection is merely a trigger of the disease, but not what causes it to continue. Or, as we believe, there might be other reasons for not finding the microbes and identifying infection as being the cause.

00:03:41
So let us look into what we believe is in this black box.
One reason for this still being a black box problem, I believe, lies in microbial detection methods. One of the more sensitive methods in routine use is PCR.
Now, would PCR detect everything?

00:04:23
The data in this graph, on the two bars to the left here, shows that when one uses a single primer to detect microbes in a given sample it misses half of what three primers can detect.
It then follows that when there is such a large difference between 1, 2, and 3 primers, the use of 4, 5, or more primers would also lead to a pretty large differences in the amount of microbes recoverable. That is to say, that using even 3 primers would miss a lot of the complexity. And that is what can be detected if the primers—if the sampling mix—are perfect, but as we know, sampling methods are not perfect. Bacteria may be hiding within cells and within biofilms.

For more on the limitations of PCR and other microbial detection methods, do have a look at our chapter in the book, Metagenomics of the Human Body.

00:05:35
Another reason for not making the possible connection between persistent infection in CFS might be that one is looking for one microbe as the cause of the disease. Now, just looking for one microbe and limiting oneself to just looking for one microbe does not make sense in the era of the metagenome.
We are asking the question: Can CFS be caused by a diverse microbiota, where the individual pathogens play a secondary role?

00:06:08
So, although the possible pathological microbiota in CFS has not been well characterized, our treatment approach has the premise that what is in the black box is a diverse microbiota.
We try to target the microbiota not by attacking it directly, but by enhancing the function of this receptor, the VDR. And amazingly, as Trevor said, this approach works! The reason it works, we believe, is that the VDR is a very key factor in innate immunity, mainly as an inducer of AMP production, anti-microbial peptide production.
While enhancement of these functions in itself could be a logical way to increase resistance to infection there are other signs that this might be particularly important.

00:06:55
One major reason for that is that several microbes are known to be associated with a reduced function of the VDR.
Rather than the microbes just having different kinds of shields against the immune system's attacks, a logical and smart alternative way not to succumb to the host's immune system would be to reduce the amount of missiles directed at them. That is to say, to disable the missile launching system, i.e., the VDR.

00:07:23
What we have done is to retarget a medication that has been on the market for some time. That medication is olmesartan. We use it at increased dosages and in a more frequent administration, something which is key to proper activiation of the VDR and to getting the clinical results that we see.

00:07:48
So basically, what this medication is doing, is to out-compete the microbial ligands for the Vitamin D binding pocket. We try to use this medication to get the patients to the finish line, that is, to get their health back.

00:08:10
Here I report the results of 64 consecutive patients—Canadian and Norwegian patients. The Canadian patients treated by a physician named Greg Blaney, which presented at the Autoimmunity Congresses before, and myself, treating the Norwegian patients.
And I would like to stress that all of patients we are currently treating are included in this cohort, whether they have been on treatment for zero years or six years.

00:08:38
Asking the patients to rate their health on a scale from 0 to 10, and defining improved as a decrease in symptoms by more than 20 percentage points, these are the results after 0-6 years. In a disease with such an overall poor prognosis as we saw earlier, I find these results very promising, indeed.
Only 2 of the 64 were in some level of gainful employment at the start of therapy. After 0-6 years of therapy 22 were working, most of them working full time. I would like to point out that this is substantially different from the average in the cohort I mentioned to you earlier, with zero patients returning to work in about the same average time frame and an average improvement in that cohort which was far below the 20 percentage points most of this cohort has reached.
11 of our patients are in the category of full recovery, which is defined as being back in full time work and essentially not having any symptoms. Since many of the patients have been on the therapy for a short time, we expect these results to improve over time in this cohort.
The dropouts are mostly early dropouts and the reason for dropping out is mainly that they found the symptom increase after starting therapy too hard to handle.

00:10:00
So this therapy gives an increase in symptoms before they get better. Why is that so?
Well, as Trevor alluded to earlier, with the killing of microbes comes collateral damage, also known as immunopathology [IP].
And IP are symptoms that arise due to microbial death and the activation of the immune system.

00:10:25
That treatments yield increased symptoms as a part of recovery of infectious diseases is not a new phenomenon. Compared to treatments for these diseases with conventional medicines, we were rather surprised to see how profoundly many of our patients were affected by immunopathology, with symptoms in many of our patients increasing severely for quite some time before getting better.
These reactions do not indicate a real worsening of the disease process, but rather the opposite, the body is finally dealing with the pathogens in an efficient way. So, we see increased symptoms as a good sign, it means that the treatment works. In fact, the severity of the reactions can be seen as a measure of just how powerful this treatment is.

00:11:25
And the effects we see can hardly be ascribed to side effects of the medication, in part because as the treatment continues these symptoms tend to disappear although they [patients] are still on the same dose of the medication.
So the immunopathology can go on for quite some time, and can be seen as a reflection of the apparent large amount of microbes the immune system has to kill.
One is looking at a treatment length of at least two-three years before recovery is achieved.

00:11:41
So, could the results we are seeing just be due to the fact that we have a long enough observation time?
It does not seem to be this way, and there are not many data on this, but in a study that I referred to here, the author of this study, Jason, had followed CFS patients for 10 years and he concludes: “The current study found that over time in a community-based sample, unbiased by help-seeking behavior, the CFS group remained rather ill with a variety of different conditions over time.”
And I might add, at the two extremes of the long term health of these patients: Out of 32 patients 4 had died, and at the other extreme, one is classified as being remitted.
So the point is, that under standard care, CFS is indeed as chronic a disease as other well known chronic diseases, and, treatment options, whether palliative or disease-resolving, are very few, indeed.

00:12:57
If you are a physician, and you would like to find out if your patients have a disturbed, non-functional VDR, what marker could you look for?
I find it useful to use vitamin 1,25-D, which is not the usual marker/metabolite of vitamin D that a doctor measures.
And as you can see here, in the study by Greg Blaney published in 2009, the 1,25 vitamin D level is indeed increased in these patients and as they progress on theapy—starting using olmesartan—you will see that this level drops, indicating that it is, indeed, a VDR agonist.

00:13:32
For more on our hypothesis do take a look at our published papers, and our book and do test our hypothesis.

00:13:41
What is needed for the future is more clinical trials to better characterize the clinical effects and to better characterize the actual mechanisms involved.
I hope some of you have found inspiration to instigate such trials.
Thank you.


Aquí la página original:
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VINCIT QUI SE VINCIT (Vence quien se vence a sí mismo)
EX NOTITIA VICTORIA (En el conocimiento reside el triunfo) 12
(tomado prestado de un amiguete... gràcies, Fran)
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DONA al Estudio de Biomarcadores para EM/SFC en el Centro de Investigación Médica Aplicada de la Clínica de Navarra:
El EM/SFC como Posible Inmunodeficiencia Adquirida https://helpify.es/comunidades/todo-por ... a-cronica/
ENTRE TODOS PODEMOS!!! :V: :V: :V: :V:

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Náufrago
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Re: Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por Náufrago » 21 May 2012, 19:04


"What we have done is to retarget a medication that has been on the market for some time."

Vamos, como la naltrexona pero con otra medicación, en éste caso el Olmesartan para aumentar el VDR....

Jo Eli, me lo he leído todo y es sumamente interesante lo que cuenta éste Sr.

El VDR no era lo que se miraba para saber si el tratamiento con el GcMaf podía ser efectivo? (que alguien me corrija si estoy muy espeso jejeje)

En éste caso no se activarían los macrófagos para que ataquen los virus y bacterias silentes, sino que se aumenta el VDR. Mismo objetivo, distintos caminos y por lo que cuenta FUNCIONA!

Creo que cada vez estamos más cerca de hacer justicia. :V:
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elipoarch
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Re: Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por elipoarch » 21 May 2012, 19:48


Sí que lo es. Se miraban otras cosas, pero el VDR era importante. Tal vez sea interesante para aquellos enfermos a quienes el GcMaf no les funcione por no tener el polimorfismo adecuado...
VINCIT QUI SE VINCIT (Vence quien se vence a sí mismo)
EX NOTITIA VICTORIA (En el conocimiento reside el triunfo) 12
(tomado prestado de un amiguete... gràcies, Fran)
___________

DONA al Estudio de Biomarcadores para EM/SFC en el Centro de Investigación Médica Aplicada de la Clínica de Navarra:
El EM/SFC como Posible Inmunodeficiencia Adquirida https://helpify.es/comunidades/todo-por ... a-cronica/
ENTRE TODOS PODEMOS!!! :V: :V: :V: :V:

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Náufrago
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Re: Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por Náufrago » 21 May 2012, 20:13


elipoarch escribió:Sí que lo es. Se miraban otras cosas, pero el VDR era importante. Tal vez sea interesante para aquellos enfermos a quienes el GcMaf no les funcione por no tener el polimorfismo adecuado...
Y no sé lo que cuesta el Olmesartan, pero seguro que es más barato que el GcMaf.... :)
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Re: Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por humbertus » 21 May 2012, 20:58


Náufrago escribió: Y no sé lo que cuesta el Olmesartan, pero seguro que es más barato que el GcMaf.... :)
El Olmesartan es aún más barato que la Naltrexona...
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Re: Tto. del SFC como inmunológico, usando inmunoestimuladores

Mensaje por Náufrago » 21 May 2012, 21:44


humbertus escribió:
Náufrago escribió: Y no sé lo que cuesta el Olmesartan, pero seguro que es más barato que el GcMaf.... :)
El Olmesartan es aún más barato que la Naltrexona...
Pues eso, surrealista. Habrá que ver si algún Dr. tiene a bien montar algún estudio con el Olmesartan o la Naltrexona, cosa que dudo porque no resultan fármacos muy rentables para las farmacéuticas y si funcionasen nos sacarían de crónicos y no resultaríamos tan interesantes para el bolsillo....
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coco
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por coco » 04 Dic 2015, 21:03


¿Alguien sabe sobre los resultados del Olmesartan?
MESTINON y L.D.N. es lo que me mantiene.

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EndSFC
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por EndSFC » 04 Dic 2015, 22:23


Vaya Coco... Buen rescate!!!! No conocía esta terapia!

Desde luego, esto es compatible con el funcionamiento del GcMAF, con las infecciones intracelulares, con la autoinmunidad y la inflamación en la patogenia del SFC, y con todo lo que apunta a una respuesta específica e inespecífica suprimida...

Aquí pego el abstract, a ver si me leo el full paper pronto:


http://www.ncbi.nlm.nih.gov/pubmed/19758226" onclick="window.open(this.href);return false;

Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease.
Waterhouse JC1, Perez TH, Albert PJ.
Author information
Abstract
Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency. Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes. The VDR dysfunction causes a decline in innate immune function that causes susceptibility to additional infections that contribute to disease progression. Evidence has been accumulating that indicates that a number of autoimmune diseases can be reversed by gradually restoring VDR function with the VDR agonist olmesartan and subinhibitory dosages of certain bacteriostatic antibiotics. Diseases showing favorable responses to treatment so far include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren's syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter's syndrome, type I and II diabetes mellitus, and uveitis. Disease reversal using this approach requires limitation of vitamin D in order to avoid contributing to dysfunction of nuclear receptors and subsequent negative consequences for immune and endocrine function. Immunopathological reactions accompanying bacterial cell death require a gradual elimination of pathogens over several years. Practical and theoretical implications are discussed, along with the compatibility of this model with current research.
"Aquel que tiene un porqué para vivir se puede enfrentar a todos los cómos" F. Nietzsche
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coco
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por coco » 04 Dic 2015, 22:25


Lo pregunto porque los de Asssem lo citan en un vídeo como terapia posible... :wtf:
MESTINON y L.D.N. es lo que me mantiene.

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Hana
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por Hana » 14 Ene 2016, 02:15


Rescato este hilo por que voy mañana al internista y no sé si llevarle esta información o no acerca del Olmesartan, se hizo algún estudio posterior o alguien del foro lo ha probado?

Gracias
#MeAction #MillionsMissing #MillonesAusentes

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Sanat Kumara
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por Sanat Kumara » 14 Ene 2016, 10:55


Hola Hana.

La semana que viene tengo cita con mi internista y voy a hacer como tu y llevarle información sobre el olmesartán.

En el protocolo marshall se usa este medicamento en dosis alta y cada seis horas.En este enlace lo explican:

http://mpkb.org/" onclick="window.open(this.href);return false;

Aunque el Doctor Mercola es bastante critico con este protocolo:

http://www.croma440.com/aclarando-la-co ... -marshall/" onclick="window.open(this.href);return false;
"La concepción materialista de la historia no tiene valor. Decir que sólo los hechos económicos y la vida material determinan y dan carácter al mundo, es una idea primaria de estudiante. La historia no se explica sólo por intereses materiales."

Pío Baroja.

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Hana
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Re: Tto. del SFC como inmunológico, usando inmunoestimulador

Mensaje por Hana » 18 Ene 2016, 23:37


Gracias por tu respuesta Sanat, a ver si tienes mas suerte que yo con el internista, por que no ha habido forma de hacerle leer nada, ni interesarse un poquito, que cerrados de mente son!

Incluso salí de la consulta pensando por que a casi todas las personas se nos exige hacer bien nuestro trabajo y los médicos cobran por dar largas a los pacientes y en algunos casos hacer mal su trabajo.

Suerte ;)
#MeAction #MillionsMissing #MillonesAusentes

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