lyme and autoimmunity

I want to organize some thoughts together later when I have more time.. but just thought it would be important to note that the term "post treatment lyme" upsets people because of how it's defined by CDC (in cahoots with the insurance industry). They say it affects some patients for a few months after treatment w abx, and that it doesn't require additional treatment to resolve. We all know (dcd too I'm sure) that this is not true and that it is the result of corruption.

Just hoping to keep the temperature low. I only mentioned it for clarity as I do not think you are defining "post treatment Lyme" in exactly the same way. I'm not saying that the term shouldn't be used.

I don't even think CDC/IDSA denies anymore that borrelia can persist.. just that the persistence is not the source of symptoms. I could be wrong...

Also trying to point out that often the reason "most people here want to argue chronic lyme is always active infection", is because the alternative means no treatment/no help (unless you want to pay an ILADS affiliated practicioner usually out of pocket).. so there's kind of an incentive to have that mindset.

Post Edited (potsnpans) : 1/12/2021 9:52:30 AM (GMT-7)

Pretty simple actually. Some people have the HLA genotype for CIRS. Others have very specific genotypes for specific diseases. The disease w/ the high predictability is actually ankloysing spondylitis. If you have that genotype, you have a 3% probability of developing AS. Not everyone develops it. The HLA type (which determines which proteins your innate immune system is primed to attack) can make you prone to developing specific antibodies. That's not enough. I could walk around my whole life w/ an antibody and not devleop disease. Antibody doesnt necessarily = disease process. Like Dr Pitts says, you need a triggering event. An infection for example that stirs your immune system. When that immune system shows up to attack the pathogen, c1q springs into action. Its like the sentinel molecule that runs around pinging antibodies and calling in for reinforcements, and while its busy signaling that there's a pathogen there, it notices the autoantibodies. "hey look, theres an antibody there, never noticed that before. What's it telling me to go after." So you need both the genetics, and the trigger. Most diseases we dont know what genes control them, but theyre there. Same w/ most PTLD.

The answers are out there, but very few drs are educated enough. Knowing what causes the disease doesnt necessarily tell you how to shut it off. Dr P goes the IVIG/immune suppression route, becuase those are the tools he's trained in. I think its possible to shut some of these disease processes off w/ lifestyle, and removal of triggers.
Trigger could be an infection or a parasite, gluten, emotional trauma, just awful lifestyle. But at the end of the day, its still an immune response, and its not always an infection thats is the perpetuating trigger. Curious people's thoughts on Dr Ps video i posted.

Post Edited (dcd2103) : 1/12/2021 10:14:16 AM (GMT-7)

Actually there are some *antibodies that do mean a disease is In process, it’s more or less a matter of time. It’s hard to say exactly when, but that’s why many antibody test have limit levels.

“In process” is like a gas peddle in an automatic transmission car. From just barely creeping forward to wide-open and anything in between.

(Edit) example: organ specific antibodies

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Post Edited (astroman) : 1/13/2021 9:06:51 AM (GMT-7)

I agree with Garzie and there's no way I could have said it better .

I might also add that the majority of patients diagnosed and treated early tend not to have a long lasting illness.. I don't know if other autoimmune triggering infections are similar...

dcd said...
Unfortunately some cases of "chronic lyme" could better be described as "post treatment lyme", in which the active infection is gone but the symptoms remain. I think that what happens in this case is that you get an infection, the infection is cleared, but the immune system is activated. It is very important to recognize that this is a possiblity. It's a very real part of lyme, and ignoring this possibility just makes no sense.

Yes it must be a possibility. Lyme certainly does cause the immune system to attack healthy cells so it's not surprising to find similarlies with diseases that are purely autoimmune (with pathogen long gone). I would guess few long term Lyme sufferers have truly cleared the infection though (as in completely eradicated borrelia burg.) Is this what you would call auto-inflammatory? .. when the bacteria is still present, even in very low levels?

The video w Dr Pitts: It's hard for me to believe he's not aware of evidence showing the persistence of bb through heavy abx protocols. I don't know why he doesn't address it, especially in a video where he claims to "solve" the controversy.. perhaps he just doesn't believe a low load would be significant in perpetuating the illness? Anyway, I don't doubt that his autoimmune styled treatments can still be effective in many scenarios.

dcd said...
The HLA type (which determines which proteins your innate immune system is primed to attack) can make you prone to developing specific antibodies.

Take a look at this study:

"Borrelia burgdorferi-Induced Changes in the Class II Self-Immunopeptidome Displayed on HLA-DR Molecules Expressed by Dendritic Cells"

https://www.frontiersin.org/articles/10.3389/fmed.2020.00568/full

Very interesting. The MHC is responsible for shifting through the protein chains and deciding what to go after. APCs (b cells, dendritic cells, macrophages) ingest foreign cells and present their proteins to T cells, which use the MHC to read said protein. I like to think that the MHC is to T-cells what an antibody is to b-cells. Basically what this is saying is that lyme alters what the APCs are willing to present, leading to confusion. Sounds similar to molecular mimicry. Very interesting. Either way, it does point to a melt-down in the immune circuitry as being the culprit. Pitts said it causes auto-reactive t-cells, which in effect is what this article is saying. If this is true, it would imply that no infection need remain to continue having problems.

I agree though, pitts is missing the fact that the infection can persist. He takes the fact that no infections can be found, and no infection symptoms are present (where's the fever, sweats and swollen lymphs, etc), only autoimmune symptoms, and bases it on that. His point is logical, and I can see why he thinks the way he does. If it weren't for the anecdotal stories I've read on this site, which have convinced me it can persist, I might believe him.

Post Edited (dcd2103) : 1/13/2021 11:47:53 AM (GMT-7)

I have come across a few other snippets that may be worth adding to the discussion:

It thinks it was Buhner that says in his Lyme book that Lyme doesn’t typically cause overt autoimmune disease - more a kind of temporary flaring of reversible auto-immune reactions that resolve once the infection is cleared/brought under control by the immune system.

I don’t know if this is an absolutely definitive statement – but the guy certainly did his research so I would guess he had a good reason for stating it - at least as a general rule.

You could certainly reason that any intracellular infection hiding inside cells would be continually opening up some of those cells( as the microbes reproduce and rupture them – the usual mode of reproduction) and thereby exposing the contents of the cell to the bodies immune system in far greater numbers than would normally be the case - including components of the nucleus - normally not seen by the immune system in any great numbers – and all the inflammation flying around would be likely to mess up the T-regs ability to do their work in preventing self-reacting antibodies.

By “true autoimmune disease” I think he is referring to something like type 1 diabetes as a frank and irreversible auto-immune condition. I have never heard of anyone recovering normal insulin control with their own pancreatic cells after having type 1 diabetes. It seems once you have it that it – your body will always make antibodies to those tissues. Even years later if they transplant some cultured insulin-producing islets cells into you ( there are experimental treatments that do this ) then they tend to last only a few months until the autoimmune process kills them off again.

I typically test positive for Anti-Nuclear Antigen antibodies ( as general auto-immunity marker ) but the pattern is speckled/non-specific and I do not test positive for any of the other specific overt known auto-immune diseases that have names – like Lupus, Sjogren’s etc .

I also test positive for dsDNA antibodies – antibodies to double string DNA - again a general autoimmune marker – but again at a low level and non-specific.
I do have Hashimoto’s – ie auto-immune thyroiditis - diagnosed by autoantibodies to thyroid tissue that occurred early in my illness - readings were into the 100’s but these have also now returned to inside normal limits - essentially zero or under the limits of the test - but that took around 2 years of diet, lifestyle changes, herbs, supplements, thyroid meds etc

These findings seem consistent with what Buhner described as going on.
The thyroid auto-immunity seems to be an odd one – mothers can get an auto-immune thyroid condition while pregnant that goes away again when they have the child – similarly a form of autoimmune diabetes can occur this way – that again tends to resolve after birth.
And there is a well-known transient thyroiditis that occurs in bed-bound hospital patients that are ill with some other illness - that I think maybe auto-immune in nature.

So these seem to be examples of auto-immune conditions that resolve when the insult is removed

Functional medicine doctors tend to teach the same concept with auto-immunity – ie that if you remove the triggers and do all the restorative stuff, it will typically resolve/ heal.
Of course exactly what those triggers are in each case and what restorative stuff you need are the million-dollar questions that drive us all around the bend! But overall, it seems to fit together reasonably well to me.

There are even some doctors who say there simply is no auto-immunity without infection = we are just not good at detecting every infection at the moment – which in the Lyme community we can well appreciate.

Many also state that hyperpermeability of the gut membrane is a pre-requisite for autoimmunity - and - well, from our discussions here – that is hardly a stretch for most of us.

Exactly which conditions are reversible and which are stuck for good like type 1 diabetes ( to my knowledge anyway ) is still very much up for grabs - there are something like 100 plus named auto-immune diseases - but in theory, the human body can make auto-antibodies to absolutely any protein in the body – and there are literally thousands of them, so we will not have names for most.

Anyway, those are musings for now - no offense - in fact, my sincere sympathy to all those with an overt auto-immune condition - its no fun having your body attack itself 😊

Garzie was curious how high your Ana is?

dcd - am just checking my ANA results

ANA dsDNA
06/2015 >1:80 0.5
03/2016 >1:100 0.3
05/2017 >1:100 0.7
09/2017 >1:160 16

don't seem to have anything later that i can find on ANA - i think at this point i was written off as having either Fibromyalgia or CFS ( dependent on which intern/registrar i saw on the day) and few further tests run - which is of course the main objective of these diagnoses.

i do have a few other auto-immune tests that were run - things like anti-phospholipid syndrome which came back negative - but some of the clotting time tests were out of whack

dcd said...
" This isnt an active infection, it's 15-20 different triggers all setting off your immune system at the same time. Point being, it's not just about spirochetes at that point, they may not even be there

I agree with your overall point- just killing spirochetes isn't going to be what gets you out of that hole. I think the more you read about borrelia though, the more you will think that they probably are there, and they likely will be indefinitely at some level.

Borrelia are mostly parisitic in nature and they manipulate a host's immune system for their own benefit. They use it to invade tissue, to break down collegenous structures for feeding.. manipulation also allows them to evade detection.

How tightly/loosely immune dysfunction mirrors the flourishing of borrelia in any given patient is still up for debate, and it probably varies a great deal.

However this underscores the importance of removing triggers and re-modulating the immune system. Not only does it bring about direct symptom resolution, it also makes it difficult for borrelia to flourish.

Garzie said...
we do know that most of the Lyme group of infections and co-infections have a surprisingly low cell count in most tissues compared to conventional acute infections...

...and for them to be considered "infections" they need to be causing "disease" (technically, I think).. with fuzzy lines everywhere it's very difficult to talk about this stuff with the language available.

Edit: didn't see dcd's post above

Post Edited (potsnpans) : 1/15/2021 7:10:37 AM (GMT-7)

Here are a couple of the studies Buhner cites while discussing infection dynamics in his Lyme book:

"Population Dynamics of Borrelia burgdorferi in Lyme Disease"

https://pubmed.ncbi.nlm.nih.gov/22470370/

From the abstract: "The chronic phase appears as an equilibration of bacterial growth and adaptive immunity."

Note: I'd expect "equilibration" to be calibrated differently across infected individuals.. and I still assume there is a great deal of variability in how symptoms surface (or if they do)

...

He writes about IL-10 in the context of a general shift away from Th1 to a Th2 dominant immune response in later stages of infection...

"Borrelia burgdorferi Elicited-IL-10 Suppresses the Production of Inflammatory Mediators, Phagocytosis, and Expression of Co-Stimulatory Receptors by Murine Macrophages and/or Dendritic Cells"

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0084980

He attributes most autoimmune-like conditions in Lyme to a polarized Th2 response, referencing lupus and systemic sclerosis.. describes this condition in Lyme as reversible because it is specifically created and modulated by the bacteria. (I believe his treatments are geared towards achieving a balance with some low level of bugs remaining, rather than total eradication).

However, he also warns that: "In long-term chronic Lyme infections, Th17 is used to modulate a combination of very high Th1 and Th2 responses... Th1 cytokines can begin to proliferate, for example, at the sites of lesions on the synovial tissue and CNS." ..This is where he cautions against the use of herbs like astragalus (which is great when used early on in infection, and for prophylaxis)...

"The problem, of course, is how to tell a long-term (mostly) Th1 semidominant, autoimmune-like process in chronic Lyme and simply a later stage of a Th2 dominant Lyme infection. Essentially, if you take Astragalus and you feel worse, you will know."

...reminds me of the danger in broadening definitions/assumptions around what is a "herx".

Post Edited (potsnpans) : 1/16/2021 6:50:12 AM (GMT-7)