thanks for taking the time to explain your thought process BrightCandle
i guess there are still many unknown factors making it really quite difficult to interpret what is happening from the data we have so far.
for instance - though there are papers detailing that ultrasound breaks up biofilm in lab tests - we don't know how much of an established biofilm colony or colonies would be broken up by the doses of ultrasound experimented so far - or if this would always leave the "seed" of a colony there afterwards.
the immune modulation via autovaccines is another area we know very little about - from our earlier discussions - it seems this mechanism was discovered and used empirically - and its still not clear why or exactly how it works - other than in the general sense that it seems to raise the immune response to the organism concerned.
thus its very hard to know how much would be enough of either of these approaches.
from my own research into biofilms i have been amazed at how resilient they are to many forms of interventions. for example
- they can form even in the storage containers of the concentrated cleaning chemicals used to supposedly remove them - eg in hospitals with MRSA
- they can form and grow in water distribution systems flowing at speeds of several metres per second - where you might expect them to be torn away from the surface they are adhering to before they even got started - eg large buildings or chemical plants
- they resist immune system breakdown - eg in chronic wounds or infected replacement replacement joints
- they resist even multiple antibiotic combinations at doses many times those needed to kill their planktonic brethren - up to 1500x normal dose in lab experiments.
the list goes on
for these reasons i am not surprised that experimental treatments might be only partially effective - or take a long time with many repeated applications.
or that the systemic symptoms might not decrease dramatically in the short term - and may even increase in the short term ( weeks or months) especially if the condition took months or years to reach its current stage - and that these signs would not therefore necessarily mean the Markov theory is invalid as the root cause mechanism. As we have no way of knowing if 5% or 95% of the biofilm colonies remain. but given how tenacious biofilms in general are known to be i would lean towards a higher percentage rather than a lower one after a few weeks of treatment.
not to argue with you or invalidate your views - just to share my perspective
i do however think that whatever treatment modalities are used - the immune system has to finish the job of clearing every last bit of biofilm - as no other known treatment has a good chance of doing that. and clearly unless that is done it seems likely the condition would relapse. so i think the autovaccine approach is very much on target from that respect.
i also think multimodal treatment strategies are also likely to be more effective than monotherapies - such as your own combination - or even ones with more layers / modes.
potential candidates for additional modes might be:
- -addition of enzymatic anti-biofilm agents
- -other biofilm disrupting agents - sugar alcohols, EDTA, lactoferrin etc
- -quorum sense (a mechanism for biofilm formation)disrupters - eg essential oils, allicin/garlic, etc
- -antibiotics or combinations of
- -hypothermia treatments - some papers suggest it helps degrade biofilms and aids microcirculation circulation
- -plant based anti-microbials - some of which have been proven effective against even drug resistant bacteria
i suspect that in many cases - as in your own -and my own - the increased symptoms in response to treatment may become the limiting factor in terms of speed of treatment.
again i have been amazed how much pain is required in my own case - to get to meaningful gain - even though the trajectory is unmistakably upward.
the latest work on ischemia reperfusion injury in ME/CFS as a probable mechanism causing PEM is one explanation that seems to fit the facts well here
also the micro clots found to contain inflammatory compounds which when broken down also cause adverse reactions to treatment is another - so this speaks to a difficult to treat without incurring exaggerated symptoms type response - and may explain the apparent asymmetry between small treatment progress with disproportionately large adverse reactions.
all just intended as food for thought
if its of any solace - i am on a kind of parallel track with a biofilm forming infectious disease - layering of multiple treatments - and only gradual improvement with much short term exacerbation of symptoms after each treatment step - but i am now also undeniably past 50% recovered. so in my own N=1 trial seems at least consistent with the above.
good luck and thanks for continuing to share your ongoing experiments!
