“The edema of the brain caused by Lyme is probably due to the blockage of the capillaries.”
(Hepatatic steatosis (“fatty liver”) can -> ideopathic intracranial hypertension. Berberine can indeed impact NAFLD).
Depakote depletes PLP (B6) and raises homocysteine levels - I can link. High levels of homocysteine can trigger "idiopathic intracranial hypertension"- I can link.
I know, for FACT...my son...CT scans proved. Genetically, he needed additional B6 as PLP, not toxic Depakote.
Healthy liver/gut...healthy mind.
I am making an educated guess...If p8 is HTLV-1, a retroviral protein, the liver takes a big "hit" from the get-go.
To study the immunomodulating activity of the HTM supernatant, the effects of the supernatant on cytokine (IFN-γ and IL-10) production by TCCs established from cells of the patient with
My sis, with lyme, almost lost her eyesight due to uveitis triggered by lyme disease.
These data show that coinfection with HTLV-1 decreases IL-5 and IgE responses in patients with strongyloidiasis consistent with a relative switch from Th2 to Th1 response.
Immunological responses such as these are important in the control of this helminthic infection.
PMID:11589779
Does HTLV-1 AND Bb infection (co-infected) do the same i.e., Th2 to Th1 response?
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Razzle
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I think Buhner says Chronic Lyme shifts the immune system towards TH2-dominance...
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4166 | From WA | Registered: Feb 2011
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Marnie
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For example, chronic Lyme arthritis is characterized by a dominant type-1 cytokine process involving particularly the T cells in the involved synovium rather than peripheral blood T cells.
On the other hand, chronic helminthic parasitic infections, and eosinophilic disorders in general, appear to be predominantly type-2 cytokine conditions.
(unable to link due to parenthesis)
The cytokine pattern of Lyme disease, and the role of Th1 with down regulation of interleukin-10 (IL-10) was first proposed in 1997.[104]
Recent studies in both acute and antibiotic refractory, or chronic, Lyme disease have shown a distinct pro-inflammatory immune process.
This pro-inflammatory process is a cell-mediated immunity and results in Th1 upregulation.
These studies have shown a significant decrease in cytokine output of (IL-10), an upregulation of interleukin-6 (IL-6) and interleukin-12 (Il-12) and interferon-gamma (IFN-gamma) and dysregulation in TNF-alpha,` predominantly.
I think co-infections may prevent the clearance...possibly ESPECIALLY p8 ...IF (big IF) it is a retroviral protein called HTLV-1.
I think we might need to consider THAT co-infection (among all the rest!).
While that retroviral protein is USUALLY "asymptomatic" it still might be doing mischief!
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Razzle
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Ok so if Lyme actually shifts the immune system towards TH1, then how come so many people experience the development of or worsening of allergies after infection with Lyme?
Also, now I'm wondering if what Buhner is thinking is TH2 dominance is actually exhaustion of the TH1 response. In other words, has the TH1 immune response "given up" after prolonged activation, which then results in a de-facto TH2 sub-dominance because TH2 can still respond when TH1 is exhausted???
I know the immune system is very complex, so maybe what I'm saying makes no sense at all. Just thinking with my keyboard...
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4166 | From WA | Registered: Feb 2011
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Marnie
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They can't mount a Th2 response to ragweed, mold, etc. Stuck in Th1 response.
Nov 14, 2013 ... Predominant *T Helper 2* Immune Responses against Bartonella...
AND...at the outset of lyme, Mg levels literally plummet and can continue to spiral down.
Mg is an anti-inflammatory and anti-histamine.
We need ATP up to drive Mg back in to lock onto ATP as Mg-ATP.
Although, if you come into contact with a particularly mean pathogen/"situation" that needs "immediate attention" (Th2) the body will do everything it can to save you and may switch responses (temporarily). Each "category" has a long list of helpers.
"Pregnancy is a complex immunological state in which a bias towards T helper 2 (Th2) protects the fetus."
Pretty good "basic" picture if you can cut, paste and make it bigger:
[ 02-26-2014, 04:46 PM: Message edited by: Marnie ]
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Razzle
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So if they can't mount a Th2 response, then is the "allergic" response based on Th1 instead??
Just trying to wrap my head around what's going on with the increased allergies and Lyme...
Thanks,
-------------------- -Razzle Lyme IgM IGeneX Pos. 18+++, 23-25+, 30++, 31+, 34++, 39 IND, 83-93 IND; IgG IGeneX Neg. 30+, 39 IND; Mayo/CDC Pos. IgM 23+, 39+; IgG Mayo/CDC Neg. band 41+; Bart. (clinical dx; Fry Labs neg. for all coinfections), sx >30 yrs. Posts: 4166 | From WA | Registered: Feb 2011
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Marnie
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The response would be to take an antihistamine because your body can't help you deal with the allergen overload.
Kids who are allergic to peanuts (genetic problem) have no way to stop the anaphylactic reaction to an antigen (protein)...they don't "put out" epinephrine as a response, so they have to grab an epi. pen.
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Marnie
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After reading the above, consider the situation where (usually older) persons become dairy intolerant. They can no longer produce the enzyme called lactase and have to take pills before enjoying a big dish of ice cream.
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