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Resveratrol and autoimmune conditions


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#1 Alistair

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Posted 05 November 2008 - 01:32 PM


There are several posts on the Resveratrol forum (if you run a search) that mention that resveratrol can exacerbate some autoimmune conditions such as rheumatoid arthritis.

I wanted to get some more detail on this and have just run a search on pubmed for 'resveratrol' and 'autoimmune'. There are five references returned for these terms, all of which say that resveratrol ameliorates autoimmune conditions.

Can anyone shed some more light on this? Are there any references that I can follow up?

Many thanks in advance.

Alistair

#2 maxwatt

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Posted 05 November 2008 - 11:47 PM

There are several posts on the Resveratrol forum (if you run a search) that mention that resveratrol can exacerbate some autoimmune conditions such as rheumatoid arthritis.

I wanted to get some more detail on this and have just run a search on pubmed for 'resveratrol' and 'autoimmune'. There are five references returned for these terms, all of which say that resveratrol ameliorates autoimmune conditions.

Can anyone shed some more light on this? Are there any references that I can follow up?

Many thanks in advance.

Alistair


The belief in this forum that resveratrol can aggravate certain autoimmune conditions is partly explained by the abastact below, and by this thread:

http://www.imminst.o...showtopic=21496

This paper:

J Rheumatol. 2008 May;35(5):804-10. Epub 2008 Apr 1. Links
Abnormal histone modification patterns in lupus CD4+ T cells.Hu N, Qiu X, Luo Y, Yuan J, Li Y, Lei W, Zhang G, Zhou Y, Su Y, Lu Q.
Department of Dermatology, Second Xiangya Hospital, Central South University, Changsha, China.

OBJECTIVE: To investigate alterations in histone modifications in patients with systemic lupus erythematosus (SLE). METHODS: Global histone H3/H4 acetylation and H3K4/H3K9 methylation in CD4+ T cells from 20 SLE patients and 10 healthy control subjects were assayed using the EpiQuik global histone H3/H4 acetylation and H3K4/H3K9 methylation assay kits. mRNA levels of 12 members of 3 classes of chromatin modifier genes were measured by real-time quantitative polymerase chain reaction. RESULTS: Global histone H3 and H4 hypoacetylation was observed in active lupus CD4+ T cells compared with controls (p = 0.002 and p = 0.009, respectively). The degree of histone H3 acetylation correlated negatively with increased disease activity in lupus patients as measured by SLEDAI (r = -0.889, p = 0.044). We found global histone H3K9 hypomethylation in both active and inactive lupus CD4+ T cells, compared with controls (p = 0.001, p = 0.003, respectively). However, global levels of H3K4 methylation were not different between patients and controls. SIRT1 mRNA levels were significantly increased in active lupus CD4+ T cells compared with controls (p < 0.001), while mRNA levels of CREBBP, P300, HDAC2, HDAC7, SUV39H2, and EZH2 were significantly downregulated in patients with active lupus (p < 0.001, p < 0.001, p = 0.01, p < 0.001, p = 0.003, p = 0.001, respectively). CONCLUSION: Histone modifications appear abnormal in CD4+ T cells in SLE.

PMID: 18398941

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#3 stephen_b

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Posted 06 November 2008 - 01:06 AM

Does anyone know of any supplements that aid autoimmune disorders?

Stephen

#4 drtom

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Posted 06 November 2008 - 01:36 PM

Does anyone know of any supplements that aid autoimmune disorders?

Stephen


It depends which autoimmune disorder you mean.
I believe that certain spices, such as curcurmin (from tumeric, also found in curry powder) have been shown to reduce the incidence and severity of MS, which is essentially an auto-immune disease (body attacks "self" by recognising myelin as "foreign").
However, they may have no effect on other autoimmune disorders.
Hope that helps.

#5 FunkOdyssey

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Posted 06 November 2008 - 04:23 PM

Does anyone know of any supplements that aid autoimmune disorders?


Yes, Vitamin D. Correcting a Vitamin D deficiency cured my mother of Sjogren's Syndrome. Of course, her overall health was still awful and the Sjogren's was just a red herring; autoimmunity is one consequence of Lyme Disease, and that's what she actually has.

A theory behind autoimmunity that is starting to prevail gives the immune system a little more credit, that it is not retarded enough to randomly attack your own body for no reason. If your genes produced immune systems programmed to self-destruct, they would not have survived the process of evolution. It begins for a legitimate reason (the pursuit of intracellular pathogens) and some confusion ensues among all of the inflammation and immune activity which results in autoantibodies to the tissue that is under fire. These disappear when the pathogen disappears.

Unfortunately, this means that the widespread prescription of immunosuppressant therapies like steroids to patients with autoimmune disorders is probably hastening their demise.

Edited by FunkOdyssey, 06 November 2008 - 04:25 PM.


#6 4liberty

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Posted 07 November 2008 - 12:18 AM

Does anyone know of any supplements that aid autoimmune disorders?

Stephen


This is unscientific, of course, but my husband (rheumatoid arthritis) and I (Crohn's disease) have both seen good results with 5-Loxin. In my husband's case, adding 5-Loxin to his regimen allowed him to taper off of methotrexate completely. He's now been two years without methotrexate (after 12 years of taking it) and still remains in a longterm remission. (He does continue to use Enbrel.) We both take 75mg three times a day.

As for resveratrol, again this is just our own experience, but we haven't found it to aggravate either of our autoimmune conditions. A couple of months ago, I switched from taking LEF's 250mg (50%?) resveratrol capsules to taking 300mg 99% micronized powder (RevGenetics). Thanks to Remicade (which I'm still using), I had been on the edge of remission for a couple of years...during these two months on the higher dose resveratrol, I have finally made it into full remission (yay!). It could be a coincidence, of course, but I can certainly say that it appears the resveratrol hasn't hurt.

Ours are both inflammatory conditions. Depending on what sort of autoimmune disorder you're trying to aid, that could make a difference. 5-Loxin is anti-inflammatory.

#7 Alistair

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Posted 07 November 2008 - 01:46 PM

Maxwatt,

Many thanks for your helpful reply. Could I summarise to see if I have understood this correctly and not missed anything?

We have some anecodotal evidence from users of this forum that resveratrol exacerbates their rheumatoid arthritis and some more anectodal evidence that resveratrol gives some people joint pain. I wouldn't normally give too much credence to anectodal evidence, but in the case of imminst users, I am inclined to give it some weight.
We have a study that indicates that people with lupus react to histone acetylation and methylation by underexpression of SIRT1 rather than upregulation of SIRT1 activity. Without resveratrol being involved.

If I haven't understood this correctly or completely, please say.

On the other hand, we have 5 pubmed studies for a search on 'resveratrol' and 'autoimmune'. Only one is on human subjects and none are particularly well designed or adequately powered. I have linked the two that I thought were most significant.

1: Harikumar KB, Aggarwal BB.
Abstract
Resveratrol: a multitargeted agent for age-associated chronic diseases.
Cell Cycle. 2008 Apr 15;7(8):1020-35. Epub 2008 Feb 15. Review.
PMID: 18414053 [PubMed - indexed for MEDLINE]
2: Singh NP, Hegde VL, Hofseth LJ, Nagarkatti M, Nagarkatti P.
Abstract
Resveratrol (trans-3,5,4'-trihydroxystilbene) ameliorates experimental allergic encephalomyelitis, primarily via induction of apoptosis in T cells involving activation of aryl hydrocarbon receptor and estrogen receptor.
Mol Pharmacol. 2007 Dec;72(6):1508-21. Epub 2007 Sep 14.
PMID: 17872969 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....pubmed/17872969
3: Shindler KS, Ventura E, Rex TS, Elliott P, Rostami A.
Free in PMC
SIRT1 activation confers neuroprotection in experimental optic neuritis.
Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3602-9.
PMID: 17652729 [PubMed - indexed for MEDLINE]
4: Penberthy WT.
Abstract
Pharmacological targeting of IDO-mediated tolerance for treating autoimmune disease.
Curr Drug Metab. 2007 Apr;8(3):245-66. Review.
PMID: 17430113 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....pubmed/17430113
5: Yoshida Y, Shioi T, Izumi T.
Free Full Text
Resveratrol ameliorates experimental autoimmune myocarditis.
Circ J. 2007 Mar;71(3):397-404.
PMID: 17322642 [PubMed - indexed for MEDLINE]

This leads me to tentatively conclude that:

Resveratrol might be both good or bad for autoimmune conditions, depending on what autoimmune condition it is. Probably rheumatoid arthritis and lupus bad and myocarditis, neurological and age-related immune dysfunction good.

I would be interested to hear if you and other people would agree with my analysis and whether you and or they can add any more value to it as I don't really feel that it is a particularly useful conclusion to those who have an autoimmune condition yet.


drtom,

I understood that curcummin was useful, but that taking it orally didn't get enough active ingredient past the liver to really count. Can you provide some links on this so I can learn some more?

Thanks in advance.


FunkOdyssey,

Thanks for your post. "A theory behind autoimmunity that is starting to prevail gives the immune system a little more credit..." I am interested to learn more on this. Do you have any links that you could let me have?

Thanks in advance.


4liberty,

Congratulations! :-)


Best regards to all,

Alistair

#8 drtom

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Posted 07 November 2008 - 03:37 PM

drtom,

I understood that curcummin was useful, but that taking it orally didn't get enough active ingredient past the liver to really count. Can you provide some links on this so I can learn some more?

Thanks in advance.

Try this for a start: www.mult-sclerosis.org/curcurmin.html
Lots of links from there.

Good luck,

DrTom

#9 FunkOdyssey

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Posted 07 November 2008 - 04:05 PM

FunkOdyssey,

Thanks for your post. "A theory behind autoimmunity that is starting to prevail gives the immune system a little more credit..." I am interested to learn more on this. Do you have any links that you could let me have?


http://roadback.org/ Look in the "Studies" area.

Almost every type of autoimmune condition has responded to antibiotic therapy. A day will come when many of these diseases are discarded entirely and named correctly for the underlying infection (be it mycoplasma, b. burgdorferi, parvovirus etc).

Edited by FunkOdyssey, 07 November 2008 - 04:15 PM.


#10 Brainbox

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Posted 07 November 2008 - 09:30 PM

Does anyone know of any supplements that aid autoimmune disorders?

Stephen

Niacinamide. I saw (I would say almost dramatic) positive results with my own eyes in a case of RA. A single anecdotal case that was inspired by:

Curr Drug Metab. 2007 Apr;8(3):245-66.Click here to read Links
Pharmacological targeting of IDO-mediated tolerance for treating autoimmune disease.
Penberthy WT.

University of Cincinnati, Cincinnati, OH 45237, USA. WTPENBER@YAHOO.COM

Cells at the maternal-fetal interface express indoleamine 2,3 dioxygenase (IDO) to consume all local tryptophan for the express purpose of starving adjacent maternal T cells of this most limiting and essential amino acid. This stops local T cell proliferation to ultimately result in the most dramatic example of immune tolerance, acceptance of the fetus. By contrast, inhibition of IDO using 1-methyl-tryptophan causes a sudden catastrophic rejection of the mammalian fetus. Immunomodulatory factors including IFNgamma, TNFalpha, IL-1, and LPS use IDO induction in responsive antigen presenting cells (APCs) also to transmit tolerogenic signals to T cells. Thus it makes sense to consider IDO induction towards tolerance for autoimmune diseases in general. Approaches to cell specific therapeutic IDO induction with NAD precursor supplementation to prevent the collateral non-T cell pathogenesis due to chronic TNFalpha-IDO activated tryptophan depletion in autoimmune diseases are reviewed. Tryptophan is an essential amino acid most immediately because it is the only precursor for the endogenous biosynthesis of nicotinamide adenine dinucleotide (NAD). Both autoimmune disease and the NAD deficiency disease pellagra occur in women at greater than twice the frequency of occurrence in men. The importance of IDO dysregulation manifest as autoimmune pellagric dementia is genetically illustrated for Nasu-Hakola Disease (or PLOSL), which is caused by a mutation in the IDO antagonizing genes TYROBP/DAP12 or TREM2. Loss of function leads to psychotic symptoms rapidly progressing to presenile dementia likely due to unchecked increases in microglial IDO expression, which depletes neurons of tryptophan causing neurodegeneration. Administration of NAD precursors rescued entire mental hospitals of dementia patients literally overnight in the 1930's and NAD precursors should help Nasu-Hakola patients as well. NAD depletion mediated by peroxynitrate PARP1 activation is one of the few established mechanisms of necrosis. Chronic elevation of TNFalpha leading to necrotic events by NAD depletion in autoimmune disease likely occurs via combination of persistent IDO activation and iNOS-peroxynitrate activation of PARP1 both of which deplete NAD. Pharmacological doses of NAD precursors repeatedly provide dramatic therapeutic benefit for rheumatoid arthritis, type 1 diabetes, multiple sclerosis, colitis, other autoimmune diseases, and schizophrenia in either the clinic or animal models. Collectively these observations support the idea that autoimmune disease may in part be considered as localized pellagra manifesting symptoms particular to the inflamed target tissues. Thus pharmacological doses of NAD precursors (nicotinic acid/niacin, nicotinamide/niacinamide, or nicotinamide riboside) should be considered as potentially essential to the therapeutic success of any IDO-inducing regimen for treating autoimmune diseases. Distinct among the NAD precursors, nicotinic acid specifically activates the g-protein coupled receptor (GPCR) GPR109a to produce the IDO-inducing tolerogenic prostaglandins PGE(2) and PGD(2). Next, PGD(2) is converted to the anti-inflammatory prostaglandin, 15d-PGJ(2). These prostaglandins exert potent anti-inflammatory activities through endogenous signaling mechanisms involving the GPCRs EP2, EP4, and DP1 along with PPARgamma respectively. Nicotinamide prevents type 1 diabetes and ameliorates multiple sclerosis in animal models, while nothing is known about the therapeutic potential of nicotinamide riboside. Alternatively the direct targeting of the non-redox NAD-dependent proteins using resveratrol to activate SIRT1 or PJ34 in order to inhibit PARP1 and prevent autoimmune pathogenesis are also given consideration.



The odd thing however is that this article also considers TRes as a possible substance wich could produce similar effects by using similar pathways. The case I was refering to did have (I would again say dramatic) negative results with TRes. So there's some quirkiness to this reasoning or maybe there are individual (genetic) influences that could play a role here. Confusing at least.

Click.

Edited by Brainbox, 07 November 2008 - 09:35 PM.


#11 FunkOdyssey

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Posted 07 November 2008 - 09:40 PM

That paper was a milestone on my journey to discover my personally held theories re: autoimmune disease. I am of the opinion now that IDO induction does help prevent autoimmunity by toning down immune activity but does not address the underlying cause which, in the case of RA would be a chronic infection of the joints. Little/no blood flow, a high degree of isolation and safety from those pesky white blood cells... for bacteria, that sounds like home sweet home doesn't it?

The CNS would be even better, if you can get in past the BBB which stops even white blood cells, its game on isn't it? Now they can set up shop for a few decades, quietly producing results like this:

J Alzheimers Dis. 2008 May;13(4):381-91.

Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes.

Miklossy J.

University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada. judithmiklossy@bluewin.ch

Alzheimer's disease (AD) is associated with dementia, brain atrophy and the aggregation and accumulation of a cortical amyloid-beta peptide (Abeta). Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a century that the spirochete Treponema pallidum can cause dementia in the atrophic form of general paresis. It is noteworthy that the pathological hallmarks of this atrophic form are similar to those of AD. Recent observations showed that bacteria, including spirochetes contain amyloidogenic proteins and also that Abeta deposition and tau phosphorylation can be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD. Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia.


Edited by FunkOdyssey, 07 November 2008 - 10:06 PM.


#12 stephen_b

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Posted 10 November 2008 - 07:52 PM

Niacinamide. I saw (I would say almost dramatic) positive results with my own eyes in a case of RA.

Interesting. Do you have any reason to suspect that nicotinic acid would be any less effective?

Dovetailing with what Funk wrote, I came across this paper by Dietrich K.Klinghardt, MD, PhD, "Lyme disease: A Look Beyond Antibiotics":

It appears that Niacin has tremendous antibiotic potential against all types of Borrelia

I'd like to get some harder information (the paper is widely circulated over the internet) on niacin's claimed antibacterial properties.

StephenB

#13 Brainbox

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Posted 10 November 2008 - 09:21 PM

Niacinamide. I saw (I would say almost dramatic) positive results with my own eyes in a case of RA.

Interesting. Do you have any reason to suspect that nicotinic acid would be any less effective?

StephenB

According to my understanding of the article linked above as described briefly here:

Both niacin and niacinamide are NAD precursors, which is the basis for their application in this context.

In addition, niacinamide also inhibits SIRT-1 (which is activated by NAD). Btw. does anyone have an idea to what the nett effect would be?
Niacin does not have this disadvantage. Furthermore, Niacin has additional anti-inflammatory benefits involving pathways not covered by Niacinamide (e.g. increasing HDL and thereby decreasing CRP).
Niacinamide has proven benefits in treatment and prevention of diabetes.
Not to forget the flush of niacin.

The reason to take niacinamide was that we were aware of other, more anecdotal evidence of the use of niacinamide in R and O arthritis and sports injury. But to take up to 2 grams of the stuff based on anecdotal evidence was a bit to steep.

But maybe a more rational choice would have been niacin because of the additional anti-inflammatory benefits. But it is also a big heuristic trial-and-error process to find something that really works, good predictions are rare. I found a time-release form of niacin (to deal with the flush), so maybe the combination of niacinamide and niacin is the next phase.

#14 Lufega

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Posted 12 November 2008 - 11:26 PM

Almost every type of autoimmune condition has responded to antibiotic therapy. A day will come when many of these diseases are discarded entirely and named correctly for the underlying infection (be it mycoplasma, b. burgdorferi, parvovirus etc).


I agree. I am seeing more and more, the use of low dose (about 100 mg) of cyclosporin to treat RA. I've always wondered what the mechanism for this was and have come up short of an answer. I then rationalized that most autoimmune disorders are probably caused by an unidentified pathogen. I prefer this idea over classifying something of "idiopathic" origin.

I hate that term.

The use of Niacin seems to be coming up again and again. I posted on the use of niacin/niacinamide to treat low stomach acid.

http://www.imminst.o...showtopic=25201

Do all forms of niacin cause liver damage or is it just the slow release form? I can't seem to get a clear answer on that.

#15 FunkOdyssey

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Posted 13 November 2008 - 05:36 AM

At a certain dose, even instant-release niacin becomes harmful to the liver. Off the top of my head, I think doses up to 2g daily of instant release niacin are safe for most people (but still require periodic monitoring of liver function). Do your own research before attempting any high-dose niacin therapy. This threshold dose is much lower with sustained or controlled release niacin.

#16 Brainbox

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Posted 13 November 2008 - 12:52 PM

In addition, niacinamide also inhibits SIRT-1 (which is activated by NAD). Btw. does anyone have an idea to what the nett effect would be?


A comment by Sinclair about this:

One must be careful when calling nicotinamide an "inhibitor" in this experiment. While it is true that our lab showed that nicotinamide is a direct inhibitor of SIRT1 enzyme, it is also a precursor of NAD+, and NAD+ is a co-substrate (i.e., activator) of SIRT1.
In vivo, there is an abundant enzyme called Nampt in cells and serum that initiates the conversion of nicotinamide to NAD+. Therefore we should entertain the possibility that nicotinamide is activating SIRT1 in vivo, not inhibiting it. This would fit with other papers showing that SIRT1 is neuroprotective.

But still Niacin does not inhibbit SIRT1, but also has a more problematic safety profile.


Both high-dose Nicinamide and Niacin would require a certain level of control and periodic bloodwork being done indeed.

Edited by Brainbox, 13 November 2008 - 12:53 PM.


#17 FunkOdyssey

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Posted 13 November 2008 - 03:30 PM

OT: anyone here taken a several hundred milligram dose of niacin before? That is an interesting experience to say the least. :) If you didn't know what to expect, I could see people rushing to the emergency room or even dialing 911 in response to the "flush".

#18 Lufega

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Posted 13 November 2008 - 07:30 PM

I've used high dose niacinamide as an anxiolytic. It is surprisingly effective. However, I also get the same results from sublingual NAD.

#19 rwac

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Posted 13 November 2008 - 07:48 PM

OT: anyone here taken a several hundred milligram dose of niacin before? That is an interesting experience to say the least. :) If you didn't know what to expect, I could see people rushing to the emergency room or even dialing 911 in response to the "flush".


I took 250 mg of Niacin once. I must say the intensity of the flush for the next couple of hours surprised me.
Not going to try that again.

#20 stephen_b

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Posted 13 November 2008 - 11:22 PM

I've been trying to up my dose lately, and I haven't made it up to a gram with nicotinic acid. After a big meal 200 or even 300 isn't really an issue. On an empty stomach, it feels like a bad sunburn for a while. The niacin flush does warm you up though when it's chilly.

Stephen

#21 anglii

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Posted 19 November 2008 - 08:57 PM

A theory behind autoimmunity that is starting to prevail gives the immune system a little more credit, that it is not retarded enough to randomly attack your own body for no reason. If your genes produced immune systems programmed to self-destruct, they would not have survived the process of evolution.

Unless, this "programmed self destruct" didn't happen until after our ancestors reproduced. Most autoimmune diseases don't rear their ulgy heads until much later than that. In my case I was 29 and pregnant with my third. However, I'd like to think that evolution would have favoured me to stick around longer inorder to protect these offspring until they were old enough to reproduce.

It begins for a legitimate reason (the pursuit of intracellular pathogens) and some confusion ensues among all of the inflammation and immune activity which results in autoantibodies to the tissue that is under fire. These disappear when the pathogen disappears.

FunkOdyssey, I would like to learn more about this model of autoimmune disease. Can you provide links, other references etc? Also, how do you propose these pathogens be made to disappear if they've done such a good job hiding/confusing the immune system.I just had a thought, years ago I read Hulda Clark's theory of how to eliminate disease. She gave detailed plans in her books (Cure for all Diseases et el) on how to build a frequency generator. Find the frequency of a given pathogen and it can be "zapped" into oblivian. Oh I wish I still had a copy.

#22 FunkOdyssey

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Posted 19 November 2008 - 09:41 PM

FunkOdyssey, I would like to learn more about this model of autoimmune disease.


Alright, one good example would be the phenomenon by which Lyme causes "multiple sclerosis" (these people really have Lyme but will usually be misdiagnosed with MS and treated incorrectly with immunosuppressant therapies):

Epidemiol Mikrobiol Imunol. 2002 Apr;51(2):60-5.
[Lyme borreliosis--incidence of serum anti-myelin antibodies]
[Article in Czech]

Rysková O, Vyslouzil L, Honegr K, Lesná J, Horácek J, Skrabková Z.

Ustav klinické mikrobiologie, UK Praha, LF Hradec Králové. ryskovao@lfhk.cuni.cz

The method of enzyme immunoassay (ELISA) was used for detection of antibodies against the basic protein myelin (antimyelin antibodies) for a group of serum samples (n 36) with positive anti-borrelia immunoglobulins IgG and IgM (ELISA-Borrelia afzelii) and their immune complexes (ELISA-PEG). Antimyelin antibodies (ELISA-Doxa Kit-Myelin Basic Protein Antibodies) were assessed in 31% (n 11) of examined serum samples of patients with the working diagnosis of Lyme borreliosis. Statistical analysis (p 0.07) confirmed a more frequent incidence of antimyelin antibodies in younger female subjects (age 31 years) as compared with a group of sera (n 25) where the authors did not record the formation of immunoglobulins against the basic myelin protein (age 51 years). Neither the value of titres nor the frequency of detected anti-borrelia IgG and IgM and immune complexes did not differ significantly in the two groups. From the assembled results ensues that in the course of Lyme borreliosis, in chronic affection of organs an autoimmune reaction may develop where the basic myelin protein is damaged (demyelinization) and subsequently antimyelin antibodies are formed.



#23 Lufega

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Posted 21 November 2008 - 06:30 PM

omit

Edited by Lufega, 21 November 2008 - 06:31 PM.


#24 sUper GeNius

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Posted 23 November 2008 - 06:35 AM

See my recent post here. I have reduced my dosage of resveratrol.

http://www.imminst.o...&...st&p=279303

#25 gattaca

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Posted 25 November 2008 - 04:57 PM

Int Immunopharmacol. 2008 Nov 17. [Epub ahead of print]Click here to read

Decreased severity of experimental autoimmune encephalomyelitis during resveratrol administration is associated with increased IL-17(+)IL-10(+) T cells, CD4(-) IFN-gamma(+) cells, and decreased macrophage IL-6 expression.

Experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple Sclerosis, is induced after injection of PLP(139-151) myelin peptide in complete Freund's adjuvant into SJL/J mice. During EAE, T cells and macrophages infiltrate the brain, produce cytokines IL-17, IFN-gamma, TNF-alpha, or IL-6, and bring about autoimmune neuroinflammation. However, infiltrating T cells which simultaneously produce IL-17 and IL-10 or infiltrating CD4(-) NKT cells that produce IFN-gamma protect against EAE. Resveratrol, a plant polyphenol, exhibits anti-inflammatory properties. To determine if resveratrol can relieve EAE, SJL/J mice were administered diets enriched in resveratrol at EAE injection. EAE symptoms were significantly less compared with controls in mice fed resveratrol. At day 56 of EAE, splenic T cells from mice fed 0%, 0.04% or 0.08% resveratrol that were restimulated with PLP(139-151) produced similar levels while splenic T cells from mice fed 0.02% resveratrol produced significantly higher levels of IL-17, IFN-gamma, and TNF-alpha. At peak EAE (day 14), mice fed resveratrol had higher numbers of IL-17(+) T cells, IL-17(+)/IL-10(+) T cells, and CD4(-)IFN-gamma (+) cells in the brain and spleen compared with controls. Adoptive transfer of day 14 EAE encephalogenic T cells into mice fed resveratrol reduced the severity of EAE. In addition, resveratrol directly suppressed expression of IL-6 and IL-12/23 p40 but increased expression of IL-12 p35 and IL-23 p19 from macrophages. Therefore resveratrol protection against EAE is not associated with declines in IL-17(+) T cells but is associated with rises in IL-17(+)/IL-10(+) T cells and CD4(-)IFN-gamma(+) and with repressed macrophage IL-6 and IL-12/23 p40 expression.

Imler TJ Jr, Petro TM.

#26 gattaca

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Posted 25 November 2008 - 04:59 PM

What I would't give to do a biopsy on those rat spleens and get a peek at who is living in the marginal zone.

#27 maxwatt

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Posted 27 November 2008 - 02:56 AM

Int Immunopharmacol. 2008 Nov 17. [Epub ahead of print]Click here to read

Decreased severity of experimental autoimmune encephalomyelitis during resveratrol administration is associated with increased IL-17(+)IL-10(+) T cells, CD4(-) IFN-gamma(+) cells, and decreased macrophage IL-6 expression.

Experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple Sclerosis, is induced after injection of PLP(139-151) myelin peptide in complete Freund's adjuvant into SJL/J mice. During EAE, T cells and macrophages infiltrate the brain, produce cytokines IL-17, IFN-gamma, TNF-alpha, or IL-6, and bring about autoimmune neuroinflammation. However, infiltrating T cells which simultaneously produce IL-17 and IL-10 or infiltrating CD4(-) NKT cells that produce IFN-gamma protect against EAE. Resveratrol, a plant polyphenol, exhibits anti-inflammatory properties. To determine if resveratrol can relieve EAE, SJL/J mice were administered diets enriched in resveratrol at EAE injection. EAE symptoms were significantly less compared with controls in mice fed resveratrol. At day 56 of EAE, splenic T cells from mice fed 0%, 0.04% or 0.08% resveratrol that were restimulated with PLP(139-151) produced similar levels while splenic T cells from mice fed 0.02% resveratrol produced significantly higher levels of IL-17, IFN-gamma, and TNF-alpha. At peak EAE (day 14), mice fed resveratrol had higher numbers of IL-17(+) T cells, IL-17(+)/IL-10(+) T cells, and CD4(-)IFN-gamma (+) cells in the brain and spleen compared with controls. Adoptive transfer of day 14 EAE encephalogenic T cells into mice fed resveratrol reduced the severity of EAE. In addition, resveratrol directly suppressed expression of IL-6 and IL-12/23 p40 but increased expression of IL-12 p35 and IL-23 p19 from macrophages. Therefore resveratrol protection against EAE is not associated with declines in IL-17(+) T cells but is associated with rises in IL-17(+)/IL-10(+) T cells and CD4(-)IFN-gamma(+) and with repressed macrophage IL-6 and IL-12/23 p40 expression.

Imler TJ Jr, Petro TM.


There seems to be an implication to the above, that there is an optimum dose: too much could be counterproductive. After googling around, I have surmised the following: if mice eat on average 5.5 grams of food a day, the .02 % resveratrol group would be getting 1.1 milligrams of resveratrol a day. If an average mouse weighs 50 grams, this translates to around 20 mg /kg. For a 70 kg human, this would be 1.4 grams. HOWEVER: for toxicity studies, doses are apportioned by a ratio that allows for the reduced metabolic rate of larger creatures, which would be around 1/5th the dose for a human compared to a mouse. So a hypothetical 70 kg human should be taking around 280 milligrams. But there are metabolic differences as well, in that humans conjugate resveratrol much more efficiently than mice. To what degree this affects the optimum dose implied by the above study, I am not sure; Neither is anyone else, I suspect. It's almost certainly more than 280 mg, perhaps 1.4 grams in the unlikely circumstance that humans' more efficient conjugation exactly cancels the mass scaling.

#28 MtnMedic

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Posted 12 December 2008 - 07:48 AM

Hello, I am new to this Forum, and this is my first post. In my opinion and from the research I have done I believe Cetyl Myristoleate is the best treatment for Rhumatoid Arthritis. I did a paper on it for a Human Biology class for my Emergency Medical degree. I have probably told over a hundred people about it, and when resveratrol came out I told everyone who could use it about it as well. The only problem is that it works in about 80% of the people. I think because it is negatively impacted by smoking and drinking coffee and Orange juice within an hour of taking it. There are only a few Human studies. But I know for a fact that it really works. Check the pubmed central and you will see two reports. You don't hear about it because it was discovered in the 60's and it is from natural plant sources, so the patents have run out.  Also search for the discoverer Dr. Harry Diehl who worked for NIH. The great thing is that it is very cheap @14$ for a 2 month supply, and there are about ten companies that produce it. 

If anyone would like to read my paper I would be happy to post it.

Cheers, Peter

#29 Brainbox

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Posted 12 December 2008 - 11:20 AM

I would be very interested. :)

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#30 nowayout

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Posted 10 February 2011 - 12:36 AM

Almost every type of autoimmune condition has responded to antibiotic therapy. A day will come when many of these diseases are discarded entirely and named correctly for the underlying infection (be it mycoplasma, b. burgdorferi, parvovirus etc).


I agree. I am seeing more and more, the use of low dose (about 100 mg) of cyclosporin to treat RA. I've always wondered what the mechanism for this was and have come up short of an answer. I then rationalized that most autoimmune disorders are probably caused by an unidentified pathogen. I prefer this idea over classifying something of "idiopathic" origin.


Cyclosporine is an immunosuppressant, so effective that it is also used to prevent graft rejection in transplants. RA is an autoimmune condition. So it makes perfect sense that cyclosporine would help it. This has nothing to do with antibiotics.
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