My CD57 cell test - possible root cause of PSSD?

General Discussion
#1

Hello guys, I received my CD57 cell test back from arminlabs, it was 44! That suggests a chronic infection, see here: https://arminlabs.com/en/tests/nk-cells-cd

It is usually seen in lyme disease, but I was negative for lyme. I tested positive IgA for several other infections though. Mycoplasma pneumoniae and Chlamydia pneumoniae can go into the CNS and cause similiar issues as borrelia burgdorferi. I think this might be my “PSSD”

According to arminlabs, low Cd57 usually means nervous system involvement, that explains cognitive symptoms. Im not sure about the accuracy of this test though, it is also seen as a “general inflammatory marker”, so maybe something else is going on, but I also have positive IgA for several infections described which can lower this test, so it seems to fit. I’m seeing a specialist soon.

To be more sure of this, I will also do a organic acid tests + microbiology test… which can test for metabolites of these bacteria

Edit: I searched this forum, one other user @vincentv also had low CD57 cells, he suspected chronic infections long ago, here might be the confirmation…

How is this possible? Seems like these drugs all interfere with our immune system, I don’t know through which pathway, maybe it is through the retinoid metabolism, SSRIs also raise cortisol in withdrawal… https://pubmed.ncbi.nlm.nih.gov/25981674/

Serotonin also changes some parameters of the immune response

Seems like these drugs put our body in the perfect biochemical alignment for chronic infection, with certain tissues beeing affected

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#2

CD57 Expression on Lymphoma Microenvironment As a New Prognostic Marker Related to Immune Dysfunction

a growing amount of evidence points toward CD57 as a marker of general immune dysfunction, independently from the underlying disease.

#3

Yeah, im sure you can find some newer research on this. Mycoplasma pneumoniae and Chlamydia pneumoniae is on the list that can lower this Cd57 count. I have tested both IgG and IgA high for both of these infections - suggesting current active infection. These are usually associated with pneumonia (which I had 1 year before pssd); but these pathogens can go intracellular anywhere, they can cause hepatitis, renal failure, go into the brain etc…

When I went to the infectiologist at my local clinic (they referred me there because my ANA titer was 1:640), they tested IgG and IgM active for those - but I had no pneumonia, they did a chest ultrasound, nothing was found. They did not agree with me to do further testing though, I told them I think this went chronic in other tissues. So I sent my blood to arminlabs.

Arminlabs is no random lab either, it’s been established in germany for years and people with lyme disease send their blood there from all over the world.

For treatment, I’m considering the “David Wheldon” treatment protocoll. It was originally made for MS.

As a test, I once took some Reishi with Oat bran, these stimulate the immune response, it totally knocked me out, normally I never sleep during the day anymore (impossible since pssd), but this knocked me out. This unloads this pathway: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/purine-nucleotide-cycle leading to increased Ammonia. My head pressure increased and I got insane fatigue, I was in bed for 4 days after this. A normal person will not get knocked out from Reishi + Oat bran. It’s about the beta glucans and tripertenes, which stimmulate the immune response potently.

I tried lowering Ammonia with L-ornithine L-Aspartate but did not have much success with it.

The windows some describe with potent corticosteroids are probably because of surpression of the immune response - which generates ROS and Ammonia itself… Mifepristone fits in here too “Mifepristone Challenge”

I don’t know where 3a-HSD fits in this theory. maybe its how the immune system gets broken in the first place. SSRI’s interfere with 3a-HSD and retinoid metabolism.

Since many tested with high progesterone, it seems like 3a HSD is downregulated.

If 3a-HSD is low, DHP could stay high, the reaction potential across 5-AR could decrease, causing progesterone to be high.

High progesterone then downregulates the sigma receptors, sigma receptors control 5ht2c receptors and more. This fits my personal experiments with DXM, a sigma agonist - it gave the most potent emotional windows so far.

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