Dr J abx combination

Hi Bhava
Dr J’s protocols are not published officially in detail anywhere online - at least not that i have found

You can get the main drugs and principles from his online presentations that are on YouTube and piece most of it together from there - but some of the specifics – like doses - are missing

in any case i think the principles are more important than the specifics for the most part – as he swaps some antibiotics out depending on patient preferences and individual cases - if you watch his presentations you will see that he is following general principles rather than being fixed on exact antibiotics

Girlie has posted her protocol from her time with him on the forum in the past so you could look for her past posts
Here is what I have been able to piece together of the persister protocol –
VIEW IMAGE

It’s not 100% - for instance the timing of the xylitol and lactoferrin is not 100% clear – could be 1st week or second week - but its likely either would work

if Girlie sees this she may be able to clarify / correct any errors

dapsone is not paired with tinidazole as such - it is in fact paired with Daraprim - as this combo is known to be effective for several target organisms - or dapsone is paired with a sulfur drug generally

Ref cystic forms – round bodies - l-forms etc - as I have posted before – I think there is confusion here - and these are essentially all the same thing – different shaped persister cells – and the different nomenclature is just a result of different people coming up with different terms for the same thing at a time when our understanding was incomplete and terminology had not yet been established
I haven’t seen anything to support that the round shaped coiled spirochetes or cysts are true cysts as produced by some parasites with an impermeable outer membrane – and are therefore differently susceptible to different antibiotics compared to the other shapes of persister cells.

instead these borrelia forms just seem to have rearranged their outer membrane from linear spiral shapes to various coiled, malformed spirals with bulb on the end or spherical shapes and as a result are susceptible to most persister drugs – like other persister cells.
At least that’s my read on it

more info here https://pmc.ncbi.nlm.nih.gov/articles/PMC2564911/

Dr J believes it targets everything except Babesia - for which he uses a separate protocol - before doing this one.

his patients have often failed treatments by other LLMDs and he has a good success rate so there is some evidence for this - i think Girlie had the three B's and recovered after his protocols after failing with a prior LLMD

i have not tried the protocol in full yet - but am working up to it

both Dr H and Dr J use protocols with multiple persister drugs in combination - so i would say the mechanism of action is basically the same.

the main difference being Dr J has demonstrated that dapsone has a relatively strong dose dependent killing response with Borrelia - including its persister cells - which is not the case with all antibiotics - at least not with increases in dose within the achievable concentrations in humans (once borrelia enter a persister state - many antibiotics do not kill more of them even if you increase the dose).
So his idea is to take advantage of this feature of dapsone by using high doses, short term - ie pulsing
however - these doses have a high side effect profile and risk profile - as you know

importantly - all indications so far is that bartonella does not have the same susceptibility to high dose dapsone as borrelia does so people are reporting doing many rounds of high dose pulse dapsone with 2 or more other persister drugs to try to resolve bartonella infections - the impression i have is that its only moderately effective for this.

yes, i believe there are only essentially
-free floating motile spirochetes
-persister cells - which may take many different morphological forms
-biofilms - which are actually aggregates of the two previous forms as colonies or microcolonies embedded in an extracellular matrix (glue like compounds excreted by the borrelia )

the boundaries are likely not black and white and the situation is in fact a dynamic one - for instance
- cells may adopt different morphological forms in response to some stressors - but remain otherwise metabolising normally - ie not strictly persister cells
or
- spirochetes may enter a persister state - ie very low metabolic activity - without necessarily changing their morphology.

in fact in any population - some individuals are always spontaneously dropping into and waking up from persister states and only the proportions change with the conditions - but the above categories are good enough for most purposes

in humans in chronic disease - its likely that the vast majority of borrelia exist in biofilm colonies distributed throughout tissues. the organism distributes itself throughout the body in the early stages of the disease - i believe its been found in every organ and every tissue.

i am doing the standard protocol Dr J uses before the persister protocol - for lyme and bartonella etc - and also doing trials of some of the persister protocol drugs to see how i respond - as i am pretty sensitive to antibiotics and dont want to overwhelm myself

the persister protocol is 3 weeks on 1 week off

yes, typically around 6 cycles - then he transitions people to the maintenance protocol - but it depends on how they are responding to the antibiotics and how they are progressing - as i understand it - if they are still herxing strongly or not making progress they may do more cycles - or he may instead look for blocking factors that have been missed

i believe he is open to using herbs - he does use things like artemisinin or artensuate ( semi synthetics based on herbs ) but i do not know the details

ok

Dear Garzie and Girlie,
thanks for your answers.
1. Garzie - in which way are you being sensitive? I have thought that herxing and intensity are basically good signs that bacteria is hit and medication is effective, so - hopefully not being masochist - the harder the hit, the better, because potentially it might shorten the time span of being ill. People speak of a possible danger of herx, but I thought it is at least some good indication - If abx do not hit, there is no herx...But perhaps you ment other type of being sensitive or overwhelmed...
2. Yes the problem of diagnosing babesia is a kind of boogyman - in spite of having negative PCR, I m never really sure if got it too or not, due to symptoms overlap. In general I feel a kind of lost in the middle of lyme and co dynamics, - what is what. Do you know if there is a kind of description of symptoms and their possible interprations?
Best wishes, B

Dear Garzie,

yes it is very clear and understandable. I also live alone. Sometimes its tough, but sofar I was not in a condition of being totally down, even though few times I thought of calling first aid or ambulance, but then things resolved somehow.

You have in the past also mentioned your abx protocol with I think Ceftin etc. But what do use for persisters? And do you have any indication that it works or you go the right direction?

If I may ask you further, can berberine be taken with food / other herbs / or has to be taken on empty stomach?

I have mostly neurological issues and join pains. It seems to me I need to use more anti-inflammatory supplements and herbs plus neuro-protective, such as alpha-lipoic acid etc etc.

Thank you
Best wishes, B

Hi Girlie and Garzie,

what is the protocol for babesia? Or at least main abx combo?

A friend from here will probably go to Dr J's clinic. Does he still see patients personally or are there other Doctors trained by him to see patients?

Best wishes,
B

Hi Garzie,

thank you very much!

It is kind that you take time and effort to answer.

Would would you advise me if I d like to be sure or to know with certainity if I have babesia or not? There are general symptoms, but it is so hard to distinguish from overlap of other infections, that I had confirmed.

Secondly, I m now trying lactoferrin with xylitol as a biofilm buster. Is lactoferrin taken solo and on empty stomach or it can be taken together with xylitol ? Is 100mg of lactoferrin twice a day too low dose? Apart from more herxing, what are the signs that it could help and work in terms of busting biofilms?

Thank you very much and again sorry if too many questions
Best wishes
B

I found a few notes

The first protocol when you’re treating Babesia/lyme
Lactoferrin/xylitol is taken
1-7 days
And on the maintenance protocol lacto/xylitol is taken on days 1,2,3
Can’t find the notes for in between those protocols
I see Garzie posted it.

everyone has an opinion Bhava

but these are based almost entirely on beliefs - not scientific trials or objective data - and most are erroneously joining up dots by filling in the blanks in their understanding of the science with personal theories based on anecdotes that seem to make sense to them (a very unreliable process).

the facts are that compared to some antibiotics it IS slightly easier for microbes to develop mutations that allow resistance to rifampicin

but even the picture that most people in the population have of antimicrobial resistance development is a misunderstanding

the scientifically verifiable fasts are:

-that even the bacterial genetic mutation for rifampicin resistance that can be made to occur in the lab in special conditions - is extremely rare in actual humans

-that even this rare event can be almost completely eliminated by using 1 or more other antibiotics in combination with rifampicin ( now the microbes must develop a precise set of 3 or more mutations at the same time to become resistant - which becomes a vanishingly small probability) - this how the WHO advise rifampicin is used in chronic bacterial infections - eg Tuberculosis - and even this is to avoid antimicrobial resistance forming at the population level - see below - rather than for the benefit of the individual patient. This is also how Dr J uses drugs in this class.

-that the real mechanism of spread of antimicrobial resistance genes is not frequent development of specific mutations in many patients in many different places over the world - but very rare events happening very occasionally around the world - that is then spread to other patients via cross contamination in hospitals and the community and then spread more widely by international air travel - (places like the WHO can track these events and the development of specific genes can often be tracked back to a single hospital on a particular date - eg the mutation that occurred in staphylococcus in india a few decades ago to create the antibiotic resistant strain called MRSA)

- that bacteria existing in persister cells and biofilm forms are over 1000 x more tolerant of most antibiotics - compared to their planktonic or non-persister forms. 1000x concentrations of most antibiotics are not biologically achievable for living humans - and as a result people with chronic infections ( that all include biofilms and persister cells ) will have no good way of differentiating true antimicrobial resistance from persister cell antimicrobial tolerance - and will frequently assume antibiotic tolerance is antibiotic resistance.

so - if people do not have the full framework within which to understand the antibiotic resistance phenomenon - or how hard even non antimicrobial resistant chronic infections are to treat - then it is natural that they will assume it is more common than it really is.


again - i hope its of some help

hi Bhava

i'm not sure how to answer those questions as i think there are some assumptions underlying them that i do not think are necessarily well founded

for instance
i do not think antibiotics should be targeted at symptoms - but selected based on targeting the infections that are believed to be present
and persister cells are a obligate feature of the biology of certain bacteria - they occur universally wherever those bacteria are found in nature - including in all humans who are infected with those bacteria - rather than to varying degree from one patient to the next.

i hope this is of some help

Yes, i track symptoms too.

But that is an end outcome.

All symptoms should improve over time if you address the infections that are the root cause.

But this does not mean there is particular value in targeting antibiotics to symptoms.
(Formal logic issue)

Thats not how they work.

So i think there is likely a flawed premise or misunderstanding in there somewhere

All the best.

i am not sure i am following you correctly Bhava

i am fully in favour of moving forward in any way one is able - and if that means focussing on one symptom at a time - then that's fine

for instance at one point i focussed on improving my sleep as a way to help my overall progress - but the tools to do this with were mainly lifestyle changes, some supplements that helped just a little, and exercise etc

things like supplements, herbs food etc can be targeted towards improving specific symptoms - like sleep

i wasn't taking antibiotics at that time - if i had they would likely have made my sleep worse while taking them but it may have improved over the long term along with other symptoms - so i don't think that can be considered as targeting one symptom.

regarding the vagus nerve theories - as far as i know modern medicines' understanding of exactly how this interacts with the immune system is in its early infancy - so i would be wary of over interpreting - but yes - i think its fair to say that anything that reduces the sense of overwhelm or stress on the patient should help their immune system function more normally - and should aid recovery in some way, and certainly, chronic stress from any cause is well established to be immune suppressive - so anything we can do to reduce it is likely to be helpful.

all the best