posted
Hello, Some sources say that Lyme is a Th1 dominant immune condition while others say it is Th2 dominant.
Buhner argues on page 72 of Healing Lyme, "However, late-stage Lyme, unlike many chronic infections, is not a Th2 dominant condition. It is Th1 dominant."
If it is truly Th1 dominant, should I not be taking supplements like noni that are supposed to increase Th1?
Any thoughts are appreciated.
Thanks, Ms. Myo
-------------------- Posts: 122 | From Texas | Registered: Jan 2005
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SForsgren
Frequent Contributor (1K+ posts)
Member # 7686
posted
From Dr. Klinghardt's protocol:
Allergy - appropriate or exaggerated immune reactions (both cellular TH1-reaction and TH2-cytokine activation). In Lyme disease often (not always)TH-1 is overly active early in the illness and can easily be downregulated by fluconazole, later TH2 becomes overly active. Nothing works better then the APN-desensitization procedure (15): while the patient is exposed to the allergen (we use a glass-carrier fixated culture of the offending microbes) the ANS is kept in a state of equilibrium, using tapping of acupuncture-points, hypnotherapeutic trauma-recall and intervention techniques and our proprietary psycho kinesiology (musclebiofeedback psychotherapy). A very effective and yet simple technique to re-regulate TH1 and TH2 back is auto-urine therapy. The patient's urine concentrates the antigens (disposed cell walls and cell fragments of offending microbes which the immune system has successfully eliminated). By passing the client's urine through a micro pore filter and injecting it i.m., the lymphocytes on patrol in the connective tissue are brought in contact with the antigen and quickly mount a specific and appropriate immune response. We use 2 ml of filtered urine once weekly for 12 weeks. All other similar approaches (autohemotherapy, homeopathic autonosodes, manipulating the immune system with supplements) are far less effective.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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-------------------- Posts: 122 | From Texas | Registered: Jan 2005
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
I've read a ton of stuff on this subject, from Paul Cheney, M. D. to Trevor Marshall, PhD., and everyone inbetween.
For me it comes down to my own experience, which is that I was strongly TH2 dominant before I got Lyme, and after 20 yrs. of being ill, I am even more TH2 dominant than before, so much so that all of my trips to the ER during this illness have been the result of allergic reactions. I had 6 last year alone, two of which required trips to the ER.
To be safe, you can avoid things that stimulate only TH1 or TH2, and take an immune modulator instead, that will help balance your immune system, no matter which way it is dysregulated. Samento is a good example of an immune modulator, and as an added bonus it also kills chetes.
Klutzo
P.S. I had the desensitization procedure done that was mentioned in a post earlier in this thread. It worked miracles for my cat allergy, but did not help my chemical sensitivities over the long run. It was well worth it though, since I love cats, and our cat sleeps in our bed.
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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posted
Recent research indicates not all autoimmune disease follows this pattern for example multiple sclerosis may be mixed or variable TH1/TH2 dominance.
-------------------- Nori Posts: 109 | From Virginia | Registered: Mar 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Sis...now 4+ years later...after 3 years of nonstop abx (list them all...) dx'd: autoimmune.
On HUMIRA ($$$ shots) to block TNF alpha - proinflammatory cytokine.
If it was a TH2 problem...she would not be on that drug!
TH1...stuck in that pathway.
These results are in line with previous experiments using cells of the adaptive immune response, indicating that strong T helper type 1 (Th1) proinflammatory responses might be associated with a successful resolution of Lyme disease.
PMID: 15958074
Rocz Akad Med Bialymst. 2005;50:173-8. Related Articles, Links
Concentration of interferon-inducible T cell chemoattractant and monocyte chemotactic protein-1 in serum and cerebrospinal fluid of patients with Lyme borreliosis.
Grygorczuk S, Zajkowska J, Swierzbinska R, Pancewicz S, Kondrusik M, Hermanowska-Szpakowicz T.
Department of Infectious Diseases and Neuroinfections, Medical University of Bialystok, Poland. [email protected]
PURPOSE: Chronic inflammation in Lyme borreliosis may be sustained by aberrant inflammatory response, characterized by Th1 lymphocyte predominance, which in turn may be determined by chemokines synthesized in inflammatory focus. The aim of the study was to evaluate synthesis of chemokines: interferon-induced T cell chemoattractant (I-TAC--chemoattractant for Th1 lymphocytes), and monocyte chemotactic protein (MCP-1) in Lyme borreliosis. MATERIAL AND METHODS: Study group consisted of 13 patients with erythema migrans, 10 with Lyme arthritis and 6 with neuroborreliosis. Serum, as well as cerebrospinal fluid (CSF) in neuroborreliosis, was obtained before (examination 1) and during (examination 2) antibiotic treatment. Control serum was obtained from 8 healthy volunteers and control csf from 8 patients in whom meningitis and neuroborreliosis was excluded after diagnostic lumbar puncture. The samples were assayed for MCP-1 and I-TAC by ELISA. RESULTS: Serum mean I-TAC concentration in examination 1 was 73.0 pg/ml in erythema migrans, 78.9 pg/ml in Lyme arthritis and 87.3 pg/ml in neuroborreliosis (29.9 pg/ml in controls, difference significant for neuroborreliosis) and did not change significantly in examination 2. MCP-1 serum concentration was significantly increased to 497.5 pg/ml in neuroborreliosis in examination 2. I-TAC concentration in csf remained low, while MCP-1 concentration in examination 1 was increased to 589.1 pg/ml, significantly higher than simultaneously in serum. CONCLUSIONS: I-TAC synthesis is increased in Lyme borreliosis and may be a factor favoring predominance of Th1 lymphocyte subset. MCP-1 creates chemotactic gradient towards central nervous system and may contribute to csf pleocytosis in neuroborreliosis.
PMID: 16358960
Bacterial lipopolysaccharides (LPS) have been postulated to play a key role in this choline deficiency model of liver injury, and LPS hepatotoxicity is mediated to a major extent by the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha).
Thus, LPS administration exacerbated liver injury induced by choline deficiency, and this injury was probably partially mediated by TNF-alpha and attenuated by anti-TNF-alpha IgG.
PMID: 9309314
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Ms.Myo, Sorry, off hand, can't think of any other immune modulators besides Samento, or at least not as good. Cumanda is a good alternate, but I believe Samento to be the best. Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96239 | From Texas | Registered: Feb 2001
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Want to modulate (change) your immune response...the route your body chose to fight this particular pathogen?
Use the tetracyclines.
But first...think about whether or not modulating your body's chosen response is the right thing to do.
TETs = tetracyclines
These results indicate that TETs are not able to act directly on the synthesis of these cytokines, but they may modulate other pathways that could in turn be responsible for the
***inhibition of IL-1 alpha and TNF-alpha synthesis.***
...evidence of the augmentation of immune responses by tetracyclines... This is the first study to show an effect of antibiotic therapy on cytokine levels in vivo.
PMID: 8331300
If you want to FEEL better, that's one thing. If you want to BE better, that's another.
Greatly simplified:
Mg drops, Ca rises, TNF alpha kicks up several notches, angiotensin II rises.
Mg OR statin/arbs drugs in HIGH doses block angiotensin II...this puts the brakes on the cholesterol pathway.
IMO, Mg is the safest way to go. Ideally our OWN Mg...which is attached to ATP inside the liver cells. Problem is...with the liver being "fatty" (due to Bb loving/needing our choline), it can't help out like it should. There are 2000 mitochondria (powerhouses) PER CELL in liver cells! Each one of the mitochondria contain Mg-ATP..which SHOULD be our "salvation"...
Get the gut healthy and the organs that help us to digest our foods and then restore the balance of the nutrients that have taken a dive.
Selenium will help lower TNF alpha...to an extent.
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