Re: Misdxd with MS, Autoimmune Issues

[Guest guest]

>

> Hi There,

>

> I just wanted to mention that I was dxd with MS 6 years ago but it was

actually Lyme disease all along. I finally saved up enough money to get tested

from Igenex and just as I suspected it came back positive even by CDC standards.

yes, I think there are many more such cases and often MS is just a specific

variety of Lyme disease, where the damage is mostly in the motor neurons. In the

neurology department where I was treated for Lyme a few years ago, there were

'MS', 'Lyme' and 'unknown' cases with all very similar symptoms. The difference

was in the docter that was treating the patient, some simply refuse to see LD

even when it is a textbook case.

I had brain damage on MRI scan that is very similar to what is seen with many MS

patients. My neurologist says he sees a difference on the scans between MS and

LD cases (the damage being more 'point-like' or elongated stretched). Other docs

say they see no difference at all.

> For those of you that have been dxd with autoimmune illnesses, the envita site

has a great video that helps explain an alternative theory about autoimmunity

that I (and lots of others on the Buhner forum) happen to agree with.

> Heres the web site:

thanks for the link, I have seen this video before and although I think the

treatment may be helpful, I think the explanation is plain wrong or at least not

supported by scientific evidence. Is Envita some sort of 'alternative' medical

center??

Where is the evidence that 'BLP' are neurotoxins that cause the LD symptoms? I

have heard the suggestion more often, but don't know any solid research that

actually proves it. Same story for other potential neurotoxins like the

lipo-polysaccharide coat, BbTox1 etc.

Where is the evidence that borrelia leave antigens in the cells that they pass

through (if I understand the video correctly), causing auto-immune disease?

I think the problem is that Borrelia antigens are sometimes very similar to

human antigens. So when the immune cells attack the Bb spirochetes there is

'collateral damage' to the host tissue. There is good evidence that this happens

with Lyme arthritis and neuroborreliosis (and probably many other

tissue-specific issues with LD).

The questions then is if the damaging immune-response persists when the Bb

bacteria are gone (in which case it could be called auto-immune) or if it will

stop when the cause (Bb) is completely eradicated (in which case it would be

just 'cross-reaction').

[Guest guest]

>

> I read an study a young woman did that 8 or 9 out of 10 brains of MS

> patients autopsied - had spirichetes in the brain tissue. Does anyone

> recall reading this?

I have never read that, and if it is true I doubt if it is representative. I

remember some studies where 30-40% of MS patients were found to have Bb

antibodies. That is much higher than for the normal population, but does not

really proof that Bb is the (a) cause for MS.

I remember that Alan Mac found spirochetes in a very high percentage of

brain autopsies from Alzheimer patients. Would be interesting to know results

for autopsies of Lyme patients and compare, but those are never done because

officially hardly anyone dies from LD ...

[Guest guest]

tnkrbell-

I am having MS type symptoms as well starting with optic neuritis 4 years ago.

Prior to that I had had a Fibro diagnosis with classic fibro symptoms for

previous 8 years. Igenx is positive (2 bands 41, 31)I seem to get worse

/crash/flare with first ramping up buhner and now recently with pharmecuticals.

I don't consider it a herx, but a crash as the first lasted 4 months with scary

neuro symptoms/nonfunctional for 4 months. Now this time with pharm drugs and

I'm far worse/very scary symptoms. My MRI during first crash was normal (that

was 2 years ago). I am also pretty chemically sensitive and sensitive in

general-so not sure if that is playing into this. The chemical sensitivities

started prior to the FMS diagnosis.

What kind of treatment have you done and did you get better/halt progression?

> > >

> > > Hi There,

> > >

> > > I just wanted to mention that I was dxd with MS 6 years ago but it was

> > actually Lyme disease all along. I finally saved up enough money to get

> > tested from Igenex and just as I suspected it came back positive even by CDC

> > standards.

> >

> > yes, I think there are many more such cases and often MS is just a specific

> > variety of Lyme disease, where the damage is mostly in the motor neurons. In

> > the neurology department where I was treated for Lyme a few years ago, there

> > were 'MS', 'Lyme' and 'unknown' cases with all very similar symptoms. The

> > difference was in the docter that was treating the patient, some simply

> > refuse to see LD even when it is a textbook case.

> >

> > I had brain damage on MRI scan that is very similar to what is seen with

> > many MS patients. My neurologist says he sees a difference on the scans

> > between MS and LD cases (the damage being more 'point-like' or elongated

> > stretched). Other docs say they see no difference at all.

> >

> >

> > > For those of you that have been dxd with autoimmune illnesses, the envita

> > site has a great video that helps explain an alternative theory about

> > autoimmunity that I (and lots of others on the Buhner forum) happen to agree

> > with.

> > > Heres the web site:

> >

> > thanks for the link, I have seen this video before and although I think the

> > treatment may be helpful, I think the explanation is plain wrong or at least

> > not supported by scientific evidence. Is Envita some sort of 'alternative'

> > medical center??

> >

> > Where is the evidence that 'BLP' are neurotoxins that cause the LD

> > symptoms? I have heard the suggestion more often, but don't know any solid

> > research that actually proves it. Same story for other potential neurotoxins

> > like the lipo-polysaccharide coat, BbTox1 etc.

> >

> > Where is the evidence that borrelia leave antigens in the cells that they

> > pass through (if I understand the video correctly), causing auto-immune

> > disease?

> >

> > I think the problem is that Borrelia antigens are sometimes very similar to

> > human antigens. So when the immune cells attack the Bb spirochetes there is

> > 'collateral damage' to the host tissue. There is good evidence that this

> > happens with Lyme arthritis and neuroborreliosis (and probably many other

> > tissue-specific issues with LD).

> >

> > The questions then is if the damaging immune-response persists when the Bb

> > bacteria are gone (in which case it could be called auto-immune) or if it

> > will stop when the cause (Bb) is completely eradicated (in which case it

> > would be just 'cross-reaction').

> >

> >

> >

>

>

>

[Guest guest]

>

> Hi ,

>

> I think I read somewhere else, and I don't remember the source, that the

> Bb spirochete is so sophisticated that it can alter its own DNA to very

> closely match the host's DNA, so that when the host's immune system

> attacks the Bb, it also attacks the host since the DNA is so similar -

> which looks like an autoimmune response.

yes, although the wording is a bit wrong here. It is better to say that it

changes its antigens so they match human antigens. The immune system does not

target DNA either, it targets products that are produced from the DNA code.

Organisms are not supposed to engineer their own DNA for such a purpose, as

normally 99% of all engineering attempts would be deadly. In the host, Borrelia

continually makes tiny, preprogrammed, changes to its DNA for generating

different antigens (e.g. VlsE and OspC). Some studies have found that after a

few months in a host, there can be thousands of genetically different versions

of the original Borrelia - but the differences in DNA are very small, usually

just one point mutation.

This process will generate new Bb surface antigens continuously (or maybe once a

month). Some of them will be so similar to human antigens that the body cannot

see the difference, or that collateral damage occurs when the immune system

targets the Bb antigens.

We know that such cross-reactions (called auto-immune by the Steere bunch etc.)

occur in Lyme Disease, you can detect strong antibody reactions e.g. in nerve

and joint tissue.

One should not assume that there is any 'conscious purpose' in making these

changes. Maybe the Bb antigen variations that are sufficiently different from

human tissue are quickly eradicated by the immune system, and only the ones that

are very similar stick because the immune attack is not effective.

Another issue is that maybe Borrelia is by design very similar to some of our

own tissues. Some scientists like Lynn Margulis think that our nerve cells and

other tubular structures used in muscle tissue etc. evolved from spirochetes.

This is similar to her original hypothesis that mitochondria in animal cells,

and chloroplasts in plant cells, evolved from symbiosis with small bacteria. The

hypothesis regarding mitochondria/chloroplast origin is by now almost

universally accepted. The spirochete origin hypothesis is much more recent and

controversial, but I think it has some good arguments.

[Guest guest]

>

>

> Re your discussion of Lynn Margolis' theories about possible origin tie-ins

between spirochetal bacteria and us, borrelia burgdorferi bacteria are anaerobic

and do best in oxygen-deficient environments. Whereas we thrive in an oxygen

environment. So it seems that we are a bit different as organisms. Just thinking

outloud about how is it we and borrelia can be developmentally connected if we

function that differently? - Robin

Borrelia are not anaerobic, they are micro-aerobic (prefer low oxygen

environment, they need some oxygen). We know that they thrive inside many types

of human cells, apparently this environment suits them well. Our 'outside'

environment is not relevant at all because the Borrelia only get to see our

inside (or the inside of the tick).

Also, this symbiosis developed probably at a very early evolutional stage,

before mammals existed so it is difficult to say what the host environment was

that they were faced with. Probably it was less aerobic than in current mammals.

Also, it could be the hypothetical spirochetal precursor had different

properties from Borrelia, among spirochetes there are very different makeups.

[Guest guest]

>

>

> By symbiosis, do you mean borrelia bacteria scavenged what they needed from

other living entities? Another Q - I thought symbiosis means both organisms

benefit. But I don't see the benefit for the nonborrelia organism. -? thx-

>

by symbiosis in this case I mean the hypothesis of an endosymbiont.

For example, plant cells gained the huge advantage of photosynthesis (harvest

energy from the sun) by allowing precursors of current chloroplast structures

inside their cells. How this symbiosis developed is impossible to say, the

'invaders', probably ancient photosynthetic bacteria, gradually lost their

independence and most of their DNA. The invaders got most of what they needed

from the plant cell, and they provided chemical energy in return. The

chloroplasts still have their own DNA, just like mitochondria have their own DNA

- a very strong argument for this hypothesis).

Yes, it should be mutually beneficial. In case of a spirochete endosymbiont the

advantage for us is clear: if they gave us our brains and muscles, they gave us

some of the biggest evolutionairy advantages ever. If true, this would put the

'auto-immune' hypothesis of Lyme in an entirely different light.