Bile can serve as a reservoir for funghi, making them harder to treat
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I think taking hesperidin / hesperitin might be one of the highest ROIs in the bioenergetic field.
I have done 3l of orange juice for a few months which apparently has 1,800 mg Hesperidin.
I didn't notice any benefits from this. If this multi factoral experiment means anything.
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@alfredoolivas I think I notice more from a hesperidin supplement than from an equivalent amount of orange juice.
I call this "the isolated compound paradox" . Happens frequently, not sure why. -
Why aren't you taking much higher doses of hepseredin and let your gut do the conversion ?
I want it to be active in high concentrations already in the lumen of the proximal small intestine for on-site support of nystatine megadosing and the azole (+ maybe NAC). If I were to not have that target I'd indeed simply buy and use plenty of the OTC capsules.
I think taking hesperidin / hesperitin might be one of the highest ROIs in the bioenergetic field.
+1. Great findings.
IMO much more promising, functional and better ROI than e.g. urolithin A or all those Mephistophelean crooked dopamine modulators far, far far downstream.
Melatonin is the other protagonist of mitochondrial health I'm currently swayed by.Had been taking 160mg of it each night for a few weeks now. The daytime grogginess btw disappeared with a combo of large-dose niacin, riboflavin, biotin and P5P. Took 3grams melatonin last night. Same effect of relaxed sleepiness from about 1 hour in but much smoother skin today. However, at such doses it appears to be the most powerful inducer of the gastrointestinal MMC I've come across and that's way too much for me in my state of being. Probably great for the on-the-brink-of-constipation folks, though. Oh boy, I do hope to become better.
Back to the fungal topic:
I'm suspecting there's something profoundly wrong with the quality of pharmacy nystatine 500,000 IU tablets. They may be consistently underdosed or super-degraded garbage. Perhaps that's why they stopped working rather than from causes within the individual.
It's a bit of a mental barrier to start assuming such but every now and then throughout the years I have come across anecdotes of other pharmaceuticals where brand or origin is of crucial difference for therapeutic response.
Raw nystatine is super sensitive and quickly degrades upon exposure to light or humidity. -
I want it to be active in high concentrations already in the lumen of the proximal small intestine for on-site support of nystatine megadosing and the azole (+ maybe NAC). If I were to not have that target I'd indeed simply buy and use plenty of the OTC capsules.
Where are you sourcing hesperitin?
Had been taking 160mg of it each night for a few weeks now. The daytime grogginess btw disappeared with a combo of large-dose niacin, riboflavin, biotin and P5P. Took 3grams melatonin last night. Same effect of relaxed sleepiness from about 1 hour in but much smoother skin today. However, at such doses it appears to be the most powerful inducer of the gastrointestinal MMC I've come across and that's way too much for me in my state of being. Probably great for the on-the-brink-of-constipation folks, though. Oh boy, I do hope to become better.
3g ?? That's wild. Did you buy it in bulk or what ? Lol
But melatonin seems to behave differently in different dosages. Although I thought high doses increase prolactin significantly. Do you notice any high prolactin symptoms ? Maybe super high doses behave differently. -
@Mauritio Yes I have it in bulk so I just grabbed my next best spoon and filled that up. It's indeed harmless. From within the EU you can get it from Lithuania via rawpowders(dot)eu.
Afaik the rise in PRL isn't chronic but only acute and like what a good night's light hygiene should do anyway. Nothing to take before any sexual or other endeavours. When I had first tested 10, 20, 30mg doses (during daytime) I felt and measured the drop in body temperature for the following hours.Hesperitin comes from the lands of pandas. Thinking that a 500mg dose should achieve a proven to be biofilm-busting 0.5-1mg/mL concentration in the duodenum and jejunum.
Nystatin is a blend of more than one molecule. Its activity is currently standardized to 5710 IU/mg in accordance with modern production techniques.
Taking two doses of 11 million IU within hours in one evening and followng up with 5 million IU four times throughout the next day has ascertained a serious chronic fungal burden.
Felt as if I wouldn't be able to bear it. Brutally strong headaches. Stiff neck. Super-high intracranial hypertension. Barely made it through two nights of not even being able to rest my head on my neck but only kind of sideways because of the intense pressure. Thought it could be a good idea to take NAC to relieve the liver of whatever but I assume it was NAC's biofilm-busting property which made things even worse. Lots of vomiting. Sort of an aseptic meningitis experience. Brutal, brutal, brutal.
Currently continueing, somewhat stable, with 2.5 million IU four times daily before daring to raise it or to add any extras. -
I've been reconsidering past supplements and their effects in the face of fungus and biofilm.
work in progress• All the B vitamins and also vitamin E quite strongly feed Candida glabrata (Caveat crucial differences to C. albicans).
• Magnesium feeds it too and the ambivalence is enhanced by its much stronger osmotic effect when mucosal absorption is impaired.
• Calcium significantly stabilizes biofilms, explaining possible initial symptom relief at the cost of long-term worsening. Perhaps even more effective against systemic effects of C. albicans than glabrata as it could temporarily "clog-up" the candidalysin etc toxins of C. albicans within the biofilm.
• Zinc and iron supplemenation feed it and greatly strengthen its biofilms. On the other hand zinc can significantly raise mucosal immune responses so it's quite double-edged; good for prolonging and intensifying any suffering even though most people need more zinc for many bodily functions.
• Copper, in contrast, is a disruptor and also raises defence mechanisms. It's quite a burden on the system but at least doesn't help out the fungus.
• Butyric acid and lactic acid act as topical biofilm disruptors and can therefore aggravate local symptoms. Nice to have endogenously as naturally prophylactic countermeasures. Caveat: C. glabrata is immensly acid-restistant.
• Alpha lipoic acid, interestingly, causes fungal membrane permeabilization at its subinhitory concentrations achievable by oral or iv. administration. I.e. it weakens fungal cells and makes them more sensitive to penetration by azoles and other antifungals or destruction by host immunity.
On the other hand, orally administered ALA exerts significant chelation of the metals and minerals like zinc and iron in the GI lumen and topically. Such sequestration significantly disrupts fungal biofilms and has the potential to aggravate local symptoms especially in the duodenum, jejunum and, if mucosal absorption is impaired by biofilms, further beyond.
Talk of ALA in the context of fungi is dominated by its half-time and redistribution issues (Cutler protocol) of toxic metals like cadmium and mercury and it is being argued by quite a few folks that these heavy metals were at the base and enablers of any chronic fungal infection. But from the aforementioned, ALA obviously has possible (over)straining impact also in the absence of pathological levels of Cd or Hg.
• EGCG binds iron, therefore a powerful biofilm disruptor especially topically; potential to aggravate local symptoms. EGCG weakens growth and resilience of Candida by inhibiting their endogenous folate synthesis.
• The major importance of (divalent) metals/minerals in biofilm composition and stability brings up the potential of oral EDTA administration as a more powerful chelation tool against intestinal fungal pools. EDTA's meagre oral absorption is of very good benefit and of relative merit over ALA's worrisome systemic heavy metal redistribution in this context.
• NAC: A powerful biofilm disruptor whilst at the same time strengthening fungi through its antioxidant properties. This is a new addition as to why NAC reliably causes diarrhea in some people.
NAC should be fine when taken with Amphotericin B or Nystatin, but not when combined with the ROS-dependent killing through azoles (study).
• Ascorbic acid / vitamin
This one also disturbs biofilms and may explain strong adverse reactions.
Important: Murine in-vivo models show that even normal daily doses of ascorbic acid (as in 200mg) will significantly counteract therapeutic success by azoles. I.e. significantly greater mortality with added ascorbic acid.
On the other hand, there's synergy of ascorbic acid with the polyene Amphotericin B as it assumedly helps to stabilize the Ampho B and prevent its early degradation. The influence was neutral between ascorbic acid and Nystatin (study).
• Enzymes: I've again been considering beta-glucanases against fungal biofilms and cell walls. Chitinases/(Hemi)-cellulases are of secondary importance. IMO the two only proper oral enzyme products against Candida are the Biofase by D & G Industries and the Ther-Biotic Interfase Plus by SFI Health / Klaire Labs. They are pricey and for some reason I keep skimping on them. I don't see great use of nattokinase or serrapeptase or fibrin targeting against fungal biofilms. However, I'm reconsidering bromelain in the face of strong past aggravating reactions to this compound. By what I can find the direct antibiofilm activity of bromelain is not so clear but most of its promises are shown against candidal adhesins. I.e. the extracellularly placed proteins used by Candida to attach themselves to surfaces and tissues.
In the face of bromelain's excellent systemic uptake and distribution I'm thinking that it may help weaken the apical attachment of fungus from the host's side at the base of their biofilms (rather than attacking the exterior layers). Bromelain appears to cover pretty much the same targets as papain: Maybe one is slightly more effective than the other but I see no need to take both. It will always somewhat irritate the mucosa, of course. Perhaps of extra benefit over papain is the dilution and degradation of mucus viscosity to increase its transmucosal cleavage of adhesins.
IME the disruptors are an everlasting pain without concurrent antifungals.
And the antifungals are (besides mostly underdosed) greatly insufficient if not combined with proper biofilm disruptors.
Current tools to use: Nystatin, an azole, hesperitin, NAC, bromelain. No or minimal supplemental minerals. Must look into EDTA (otherwise EGCG or ALA on an empty stomach).Addendum 1:
There's tetrasodium EDTA/edetate which is alkaline and disodium edetate which is slightly acidic.
The disodium form would seem to be more sensible to pass through the stomach. It's freely and cheaply available.
In contrast, for i.v. use it's always calcium disodium EDTA as it is supposed to release its pre-loaded calcium ion upon facing the greater binding affinity of a heavy metal ion. Quite necessary for i.v. use to lower acute cardiovascular risk and bone loss but it makes no sense for oral use against biofilm as one would explicitely want to sequester also calcium.
There was one poster one reddit 8years ago reporting on using disodium EDTA and feeling initial symptoms already from a mere 50mg before eventually creeping it up to 300mg once per day. Better to start humbly then.
Addendum 2:
Definitely encapsulate any oral disodium EDTA. It's not very acidic but obviously readily grabs calcium. If you know how freshly mineralized teeth feel: Having drunk 2Na-EDTA dissolved in a glass of water, even after an immediate extra rinse, feels like the opposite of that. -
Had a hunch that grapefruit seed extract (GSE) may be a good thing against fungi.
Didn't realize before that the active bioflavonoids in GSE are essentially all naringin (and a fraction of hesperidin).Naringin at 400µM which is about about 0.23mg/mL (?) destroys mixed dental caries (cavities) biofilm in vitro.
That's about 10 drops of high-quality GSE in half a teaspoon of water. GSE's quite a good thing for dental and oral care then.
Would like to see the full text to see the specific results of the other bioflavonoids: curcumin, quercetin, morin, rutin, and hesperetin.
Prevalence and eradication of mixed biofilms of Streptococcus mutans and Candida albicans using naringin: In vitro and in silico investigations, 2026 -
@CrumblingCookie This confirms what some light research revealed for me a few years ago, on GSE. I have it on my list of ingredients for a homemade toothpaste.
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Have grazed the RPF reservoirs once again about fungi.
The absolute most knowledgable posts IMO came by user Sergey. Hoped to find more from him about it all.
Maurition has been the most persistent poster of related studies and bits on fungi throughout impressively many years. There was also interesting, productive interplay between amazoniac and Travis yet he was too focused-in on C. albicans exclusively. As are all the easily misleading megadosing B2, B3, aspirin contributions by haidut (false generalization of candidal species).
User narouz had been one of the most trying (as far as forum posts can tell) to get a grip of his fungal burden for many years.Alas, the persistently active and concealed Candida species in diseases of a chronic course are mostly C. parapsilosis, C. tropicalis, C. glabrata.
Plus chronic persistence of Aspergillus fumigatus as a superior perpetrator in specific disease types.
Plus the other odd fungi / mycobiome found in brain tissues, neurodegenerative diseases and also distinctly present in tumor tissues but not in tumor-surrounding healthy tissues and blood of the same people. -
L-form, aka protoplast or spheroplast, yeasts and fungi are likely the much more widespread and pressing issues next to biofilms. IMO of a more widespread importance than the specialty case of additional biliary survival as per this thread's original topic.
Such L-form variants (predominated by filamentous Aspergillus, plus Candida parapsilosis and others) were found in autistic children, and often their mothers yet not in healthy controls.
Acquisition of the L-forms especially during gestation and infancy is suspected to confer a particular kind of life-long immunological blindness to these.
Dysbiotic microbiota in autistic children and their mothers: persistence of fungal and bacterial wall-deficient L-form variants in blood, 2019An according collection of case studies, albeit with a strong conflict of interests (authors are heavily involved in Mosaic Diagnostics, formerly Great Plains Laboratory, with their urine organic acid tests):
Case Study: Rapid Complete Recovery From An Autism Spectrum Disorder After Treatment of Aspergillus With The Antifungal Drugs Itraconazole And Sporanox, 2020
The seemingly most powerful antifungal combination discovered so far which targets the fungal membranes and therefore equally well any L-form persister fungi variants
is Itraconazole or Posaconazole + a HIV protease inhibitor like Atazavir (+Ritonavir as a systemic inhibitor of degradation via Cyp3A4 to boost ATV's impact. RTV can be very cheap; thus no biggie):Enhanced antifungal activity of posaconazole against Candida auris by HIV protease inhibitors, atazanavir and saquinavir, 2024
There are a few more studies published on combinations like this without the particular use of spheroplasts but on "normal" fungi, too.
Such combos also overcome aquired resistancies by upregulated efflux pumps (CDR1/2) and the filaments and biofilm abilities. @sunsunsun -
B BearWithMe referenced this topic
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