Low dose abx therapy

[Guest guest]

Barb:

Thanks good work, I changed the subject line.

I would like understand why/who low dose abx helps as i believe that it

can be benefial for alot of as understanding

what is a low dos ? Or rather what happens att different dosage ?

Some of my experince and thougths

My allergy has changed I haven't and I havn't touched a pill for it the

last 3 years.

Before that I have used many a lot of allergy medication and still more

or less stayed in bed for 7-14 days each spring.

In sweden this is one of the worse allergy springs for many years.

Low dos and/or pulsed abx is very interesting. This is my 18 month

observation

For me it stablize the body. All my symptoms is more or less there and

the effect of them is getting smaller.

I react and recover within hours instead of weeks or months instead of

getting worse and worse.

The reaction is less and usually not pain killer or other meds is

needed, just rest.

I function much better and there is limits, when getting outside of them

i'm back with as before.

Problem is that i don't know were the limits are, they move and when I'm

starting to be more active I get into

unkown terretory.

*Anthroposoph medicine thinking targets the body and inderectly the

bacteria, they have a good reputation for

dealing with chronic illness. This would indicate that there is more

than one way of doing it.

*I get suspected immun reaktion(IgE) on the skin I talked to the lab

that did the* Phadiatop* testing and she said that the

this reaktion disapear within minuts if when what I react on is removed.

This is is a blood test that is the same

as the allergy tests done one the skin

http://provtagningsanvisningar.karolinska.se/templates/Provanvisning____57254.as\

px

This testing was done in 1990ies

The reaktion is like a small red dot/bulb (like a insect sting) with a

read area surrounding it and itching

like hell.

This 'adiatop' and no flu, and allergy thing indcate that something is

happening with the immun(controll) system.

What is the english word for adiatop (it's describe as a skin

sensitivity and it's IgE polmonary respons)

Consider a bacterial load distributed in the whole body, at some points

you will get lower concentration.

1,25D are local, inflammations are local -?> are bacterial local ?? and

what is really antibiotic resistance in

the body. See also what Broson and Brorson writes about abx

concentration for differnt froms of BB.

Reading L Mattmans book, i find that many bacteria(all??) have differnt

form and that form have differnt properties

this may be for survival ? If a bacteria has survival(for its kind) as

it's main property each individaul may be easy

killed but not the population in the body.

The property of not beeing detected for a long time allows for a good

distributaion in the body.

Being there for a long time allows for adjustment of the controll

system(endocine,neuro, immun) to its favor.

This may also allow for other bacteria to profit.

What IF changing the circumstances for all this is key, not the ability

to kill or inhbit a certain bacteria ?

This may explain why rife,zapper,low dos abx, mp and other terapies work.

/Per

Barb Peck wrote in Re: Looking for THINKERS and I know you are here

(Jelly & Per- Low dose)

06/11/2006:

>Per:

>

>Low-dose therapy is used in a few conditions.

>What we call low dose is important though, because the DOSE will

>determine if it kills bacteria, keeps them im colony form, or is SO

>low that there isn't any antimicrobial effect what so ever.

>

>In the immunosuppressed, where bacteria has to be controlled, the

>lowest dose possible is found, and that is gievn as infrequently as

>possible.

>See reference 1

>

>In other conditions, with low doses, that are UNDER the threshold that

>does anything to bacteria- it's the enzyme inhibitory effects of the

>abx that's helping. And there are drugs being developed based on the

>tetrcycline family that retain the inhibitory effects, and totally

>lack the antimicrobial effects.

>

>So- in essence - I think different things happen at different doses..

>and it's all NOT about killing bacteria and herxing. Without further

>researching I do not know where the cutt-offs are with dose, but the

>low dose for mouth disorders is about 20 mg... so a 3 mg dose isn't

>going to have any anti-microbial properties... but who knows- maybe

>it inhibits MMPS even at that dose.

>

>See refernce 2 on enzyme inhibition

>

>

>

>

>Antimicrob Agents Chemother. 1992 October; 36(10): 2328–2330.

>

>Low-dose trimethoprim-sulfamethoxazole alone and in association with

>zidovudine for prevention and treatment of murine Pneumocystis

>carinii pneumonia.

>M Brun-Pascaud, P M Girard, and J J Pocidalo

>

>Institut National de la Santé et de la Recherche Médicale, U. 13,

>Hôpital Claude Bernard, Paris, France.

>

>Low-dose trimethoprim-sulfamethoxazole (TMP-SMX) alone was found to

>be as effective as low-dose TMP-SMX plus zidovudine and standard-dose

>TMP-SMX alone in preventing and treating Pneumocystis carinii

>pneumonia (PCP) in an immunosuppressed-rat model. Zidovudine alone

>had no preventive or curative effect on PCP. We conclude that the

>initially reported reduced incidence of PCP in human immunodeficiency

>virus-infected patients treated with zidovudine alone is not due to

>anti-P. carinii activity of zidovudine. Furthermore, the clinical

>efficacy of low-dose TMP-SMX for the prevention and treatment of PCP

>should be further investigated

>

>http://www.pubmedcentral.gov/articlerender.fcgi?artid=245497

>

>REFERENCE 2

>J Periodontol. 2004 Mar;75(3):453-63

>Subantimicrobial dose doxycycline efficacy as a matrix

>metalloproteinase inhibitor in chronic periodontitis patients is

>enhanced when combined with a non-steroidal anti-inflammatory drug.

>

>Lee HM, Ciancio SG, Tuter G, ME, Komaroff E, Golub LM.

>

>Department of Oral Biology and Pathology, School of Dental Medicine,

>State University of New York at Stony Brook, Stony Brook, NY 11794,

>USA.

>

>BACKGROUND: Administration of subantimicrobial dose doxycycline (SDD)

>to chronic periodontitis (CP) patients has repeatedly been found to

>reduce mammalian collagenase and other matrix metalloproteinase (MMP)

>activity in gingival tissues and crevicular fluid, in association

>with clinical efficacy, without the emergence of antibiotic-resistant

>bacteria either orally or extra-orally. More recently, SDD adjunctive

>to repeated mechanical debridement resulted in dramatic clinical

>improvement in patients (>50% smokers) with generalized aggressive

>periodontitis. As an additional pharmacologic approach, non-steroidal

>anti-inflammatory drugs (NSAIDs) can reduce gingival inflammation and

>alveolar bone resorption, at least under experimental conditions. In

>the current study, we determined the effect of administering a

>combination (combination) of these two host-modulating drugs (SDD

>plus low-dose NSAID) to CP patients, on selected neutral proteinases

>in gingiva, enzymes believed to mediate periodontal breakdown.

>Earlier preliminary studies in humans with bullous pemphigoid, which

>is also associated with excessive levels of host-derived proteinases

>including MMPs, indicated improved clinical efficacy of combination

>therapy. METHODS: Nineteen CP patients, scheduled for mucoperiosteal

>flap surgery bilaterally in the maxillary arch, were randomly

>distributed into three experimental groups administered either 1) low-

>dose flurbiprofen (LDF) alone, 50 mg q.d.; 2) SDD (20 mg b.i.d.)

>alone; or 3) a combination of SDD plus LDF (combination). The

>gingival tissues were biopsied during surgery from right and left

>maxillary posterior sextants, before and after a 3-week regimen of

>medication, respectively. The tissues were then extracted, the

>extracts partially purified, then analyzed for the endogenous

>proteinase inhibitor, alpha1-PI, and its breakdown product, and for

>host-derived matrix metalloproteinases (i.e., collagenases,

>gelatinases) and neutrophil elastase activities. RESULTS: Short-term

>therapy with SDD alone produced a significant reduction and LDF alone

>produced no reduction in host-derived neutral proteinases. However,

>the combination therapy produced a statistically significant

>synergistic reduction of collagenase, gelatinase, and serpinolytic

>(alpha1-PI degrading) activities (69%, 69%, and 75% reductions,

>respectively) and a lesser reduction of the serine proteinase,

>elastase (46%). CONCLUSIONS: Consistent with previous studies on

>animal models of chronic destructive disease (e.g., rheumatoid

>arthritis), the SDD and NSAID combination therapy synergistically

>suppressed MMP and other neutral proteinases in the gingiva of CP

>patients. A mechanism, suggested by earlier animal studies, involves

>the NSAID, in the combination regimen, increasing the uptake of the

>tetracycline-based MMP inhibitor in the inflammatory lesion, thus

>synergistically enhancing the efficacy of this medication.

>

>Publication Types:

>Clinical Trial

>Randomized Controlled Trial

>

>PMID: 15088884 [PubMed - indexed for MEDLINE]

>

>

>