Candida Overgrowth. What To Do Now?

[haidut]

LDL also seems to promote fungal infections. In LDL receptor knockout mice, which have high levels of LDL, there is decreased resistance to Candida (37, 38).

Actually, that statement does not imply LDL promotes Candida growth. It is complete insensitivity to LDL which promoted the Candida growth. The high LDL is a side effects of that sensitivity, but LDL itself is probably not growth-promoting.

 

[Prosper]

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[Travis]

Okay, after lots and lots of research and experiencing a huge variety of symptoms, I finally conclude that I suffer candida overgrowth, not appendicitis.

I experience die-off symptoms, candida stools, fever, chill, depression, brainfog, dandruff, flakey skin on my face etc. I've been consuming 3g of aspirin + 1.5g of glycine + lots of vitamin k2 everyday for 6 days to clean off the candida off my gut. I had to quit yesterday (the 6th day) because it came to the point that the aspirin hurts my stomach even with the help of glycine.

I get the aspirin idea from this thread: https://raypeatforum.com/community/threads/aspirin-as-an-antifungal-drug-even-against-candida.6764/

I don't know what to do with my diet anymore. Some people say sugar and fruit are bad since they feed candida. Some says that starch is bad. Some says that white rice is bad but brown rice is good. Anti-candida says remove carb out of the diet but glucose removal makes metabolism worse and worsening candida overgrowth.

Some says it's better to make your gut sterile, but others say it may be better to keep candida in stomach but balanced with other bacterias.

I'm confused. Very confused.

My diet is currently 50% lean organ meat, 30-40% green vegetables, 20-10% carbs. I no longer consume dairy products. I'll get enough calcium from green vegetables.

I have to be careful with the carbs part. Which one I can and can't consume. I have orange juice, sugar and raw honey laying around in my fridge and kitchen yet I'm cautious about consuming them in fear of candida flaring up. The only carb I consume is brown rice, since it has lower GI and doesn't feed candida (so they say online)...

My current supplements:

Vitamin B1, b2, b3, b5, p5p, biotin, c, LE Super K (K2), liposomal glutathione, epsom salt bath, ionized magnesium, l-carnitine, l-lysine, MSM.

Potassium iodide in high milligram doses, per day, is an effective way to go about this. This is because the iodide ion (I⁻) is oxidized by neutrophil peroxidase to hypoiodite (IO⁻), the most effective immunogenic small molecule against yeast cells. This has been experimentally-confirmed, and very likely why potassium iodide has been reported as being effective in clinical case reports. Although myeloperoxidase can oxidize other halogens, such as chloride (Cl⁻) and bromide (Br⁻), the kinetic rates of formation are much lower for these ions. Thiocyanate can also be used, forming hypothiocyanite (SCN⁻), yet this is similarly less-effective than the hypoiodite (IO⁻) product.

The order of oxidative potential is as follows: SCN⁻ > IO⁻ > Cl⁻ > Br⁻.

Although hypocyanite (SCN⁻) is a more powerful oxidant, it is formed at a far lower speed than hypoiodite (IO⁻). What also makes the iodide ion (I⁻) product particularly effective is its high pKa, meaning that the HIO ⇌ IO⁻ equilibrium lies far to the left. Hypoiodite is actually the only hypohalogen—or pseudo-hypohalogen in the case of SCN⁻—that exists primarily in the neutral protonated state. This fact, along with the polarizability of the large iodine ion, would be expected to give hypoiodous acid (HIO) a far greater membrane affinity than the other myeloperoxidase products. It is in this location that hypoiodous acid oxidizes cell membrane chitin and yeast β-glycans, forming insoluble compounds and subsequent membrane pores. This reaction forms the basis of classic chemical test: When determining the extent of aldehyde groups on cellulose—another β-linked polysaccharide—hypoiodite is the only hypohalogen ever used. The iodide ion also has a natural affinity for polysaccharides, a phenomenon that forms the basis of another classic test: The starch–iodide reaction, commonly used to detect counterfeit money.

The established capacity of iodide to destroy yeast in vivo occurs in concentrations far lower than those required for a direct inhibitory effect. Although you hear talk that thyroid hormone could be responsible for these effects, this is just a knee-jerk assumption made by people unaware of neutrophil myeloperoxidase. I would expect Armour thyroid to be far less effective against C. albicans.

 

[Wagner83]

Potassium iodide in high milligram doses, per day, is an effective way to go about this. This is because the iodide ion (I⁻) is oxidized by neutrophil peroxidase to hypoiodite (IO⁻), the most effective immunogenic small molecule against yeast cells. This has been experimentally-confirmed, and very likely why potassium iodide has been reported as being effective in clinical case reports. Although myeloperoxidase can oxidize other halogens, such as chloride (Cl⁻) and bromide (Br⁻), the kinetic rates of formation are much lower for these ions. Thiocyanate can also be used, forming hypothiocyanite (SCN⁻), yet this is similarly less-effective than the hypoiodite (IO⁻) product.

The order of oxidative potential is as follows: SCN⁻ > IO⁻ > Cl⁻ > Br⁻.

Although hypocyanite (SCN⁻) is a more powerful oxidant, it is formed at a far lower speed than hypoiodite (IO⁻). What also makes the iodide ion (I⁻) product particularly effective is its high pKa, meaning that the HIO ⇌ IO⁻ equilibrium lies far to the left. Hypoiodite is actually the only hypohalogen—or pseudo-hypohalogen in the case of SCN⁻—that exists primarily in the neutral protonated state. This fact, along with the polarizability of the large iodine ion, would be expected to give hypoiodous acid (HIO) a far greater membrane affinity than the other myeloperoxidase products. It is in this location that hypoiodous acid oxidizes cell membrane chitin and yeast β-glycans, forming insoluble compounds and subsequent membrane pores. This reaction forms the basis of classic chemical test: When determining the extent of aldehyde groups on cellulose—another β-linked polysaccharide—hypoiodite is the only hypohalogen ever used. The iodide ion also has a natural affinity for polysaccharides, a phenomenon that forms the basis of another classic test: The starch–iodide reaction, commonly used to detect counterfeit money.

The established capacity of iodide to destroy yeast in vivo occurs in concentrations far lower than those required for a direct inhibitory effect. Although you hear talk that thyroid hormone could be responsible for these effects, this is just a knee-jerk assumption made by people unaware of neutrophil myeloperoxidase. I would expect Armour thyroid to be far less effective against C. albicans.

What about a pineapple fast to clean the gallbladder in the process and catch two bards with one stone?

 

[michael94]

.

same

 

[Travis]

What about a pineapple fast to clean the gallbladder in the process and catch two bards with one stone?

Yeah, the iodide ion should synergize with everything. Even the amount found in kelp should be helpful, as studies on coastal Japanese imply that iodide ions bioaccumulate in the extracellular space—ostensibly ionically-bound to glycogen. We all have a 'body store' of iodide, and although I'd hate to make the analogy to mercury it seems appropriate in this case. Giant ions like iodide, gold, and mercury have a very extensive and polarizeable electron valence, a property makes them more lipophilic and fat soluble—and their high-mass nuclei gives them inertia. Iodide ions are unique in their affinity for polysaccharides, so besides cell membranes you'd expect them to also accumulate in the extracellular space.

 

[inthedark]

Yeah, the iodide ion should synergize with everything. Even the amount found in kelp should be helpful, as studies on coastal Japanese imply that iodide ions bioaccumulate in the extracellular space—ostensibly ionically-bound to glycogen. We all have a 'body store' of iodide, and although I'd hate to make the analogy to mercury it seems appropriate in this case. Giant ions like iodide, gold, and mercury have a very extensive and polarizeable electron valence, a property makes them more lipophilic and fat soluble—and their high-mass nuclei gives them inertia. Iodide ions are unique in their affinity for polysaccharides, so besides cell membranes you'd expect them to also accumulate in the extracellular space.

This is very interesting, what doses do you think would be effective?

 

[A. squamosa]

what's a candida stool?

 

[Travis]

This is very interesting, what doses do you think would be effective?

All of them, and with efficacy increasing proportional to dose.

 

[inthedark]

All of them, and with efficacy increasing proportional to dose.

Thanks. What would you consider a "high milligram" dose for potassium iodide in this application?

Also, I wonder if aspirin + potassium iodide would make a good protocol for yeast issues? (Aspirin As An Antifungal Drug, Even Against Candida)

 

[Travis]

Also, I wonder if aspirin + potassium iodide would make a good protocol for yeast issues? (Aspirin As An Antifungal Drug, Even Against Candida)

Aspirin certainly does work in vitro, as do COX inhibitor in general. Studies demonstrating aspirin-inhibition substantiate the metabolic studies on yeast lipid-production and prostaglandin signalling, and also imply that omega−6 fatty acids would tend to promote yeast. The fruitarians who had largely eliminated Candida through eating only raw foods are often observed to complain of 'nuts interfering with the process.' The omega−6 fatty acids could certainly be why, a fact that would completely exonerate macadamia and coconuts.

 

[CDT]

Would you mind elaborating on your symptoms and have they healed to any degree since your post.

 

[CDT]

Also, to anyone who has browsed this post before, ful blown candidiasis may not be the issue, but I was wondering if minor upsets (gut dysbiosis) might be the concern, and if so, what is the way to treat this? I am currently suffering from a presumptuous dysbiosis and must mention that I am a vegetarian. What kinds of things should I incorporate (restriction diet methods, vitamin C flush) etc. would you all recommend for minor dysbioses?

 

[Lewistx]

Im having severe infections and thinking of using msm i got hpylori abd and metronidazole doesn't work I know i have fungi too because my toenails are infectected

I think now that hypothyroid is the result of candida overgrowth, at least in my case. The thyroid can't get all the nutrient/hormones it needs if liver and kidney are suppressed by candida.

I can't permanently fix thyroid if that uninvited organism lives in my gut wrecking havoc to intestinal wall, liver and kidney. The candida needs to be flushed out to near zero then get my liver and kidney back in the game again. Then it'll be a lot easier to heal hypothyroidism from that point on.

Right now I'm kinda low carb again, eating only brown rice for carbs in order to not feed candida. I've also been flushing them out with 300mg niacin + vitamin B complex + hydrogen ionized water + MSM. The die off was insane within the first week, but it lessens now. The stool also shows lots of dying candida. So I'm on the right track so far.

 

[Daniil]

I think the excessive growth of candida is really a problem. Otherwise, where do all these mysterious symptoms come from in people? There is no smoke without fire, as they say.

I have seen a study in which garlic extract was as effective against candida as nystatin. I had problems that I associated with candida, and they went away after adding raw garlic. The iodine didn't help. But after the iodine, some accumulations of bacteria/small parasites came out of me.

 

[johnwester130]

nyastin looks promising??

flower of sulfur powder?

flowers of sulfur looks easier and cheaper, use it like baking soda.

 

[Peatness]

Evaluation of the antifungal activity of olive leaf aqueous extracts against Candida albicans PTCC-5027 - PubMed

In this study, antifungal property of olive leaf extracts against <i>Candida albicans</i> PTCC-5027 was examined. Fresh olive leaf extracts were prepared using distilled water in a Soxhlet apparatus. The antifungal activity of the extract was analyzed by measuring the minimum inhibitory...

pubmed.ncbi.nlm.nih.gov

manganese – Page 2 – Diary of Unknown Symptoms

Posts about manganese written by aaronjreid

aaronjreid.wordpress.com

 

[Vins7]

No you don't.
Unless you get a positive stool test for candida albicans from a doctor or your mouth looks like the picture I posted below you do not have candidiasis. Real candidiasis outbreaks generally only occur in severely immunosuppressed people and are resolved with a few days of antifungal drugs. We all have the candida yeast in our body but even a moderately healthy immune system keeps it in check (much like the dormant herpes virus).

A white coating on the tongue is NOT oral candidiasis, it's just an overgrowth of relatively harmless other yeasts that live in your mouth. For me it's usually caused by maldigestion because you don't chew your food (especially starches) properly, you gulp down cold liquids during a meal, you eat things that are hard to digest in general, improper combination of macronutrients etc.

F.uck that whole anti candida alternative health fear mongering bull****, it's a small industry created to scare people and sell them useless supplements.
Been there, done that, ruined my health even more with that low carb antifungal fasting cleanse nonsense.

I've not looked at your other threads and don't know your current health problems but trust me, this whole candida thing is not the answer

The reality ????

 

[Amazoniac]

I thought that I had shared these before, but couldn't locate:

- Mechanistic Understanding of Candida albicans Biofilm Formation and Approaches for Its Inhibition
- Antifungal Compounds against Candida Infections from Traditional Chinese Medicine

- How alkalinization drives fungal pathogenicity

Spoiler

"[..]the human pathogen C. faddicans raises the pH in host macrophages by several units, resulting in neutralization of the normally acidic phagosome [19, 20].

The main mechanism of host alkalinization reported in these fungal species is the release of ammonia, which acts as a weak base [17, 19]."

"In C. faddicans, an upshift in pH promotes the transition from the unicellular yeast to the filamentous hyphal form [4, 8, 19]. This morphogenetic switch, which is critical for virulence in mammalian hosts, is mediated by a number of cell signaling pathways, including the Pal/Rim route and the invasive growth (IG) mitogen-activated protein kinase (MAPK) cascade [8, 32]."

"Phytopathogens have been traditionally classified into acidifiers and alkalinizers based on their strategy to either decrease or increase the pH of the surrounding host tissue during infection [3]. However, this distinction might be less clear-cut than previously assumed. A recent study involving different fruit-infecting fungi revealed that each of them could induce either alkalinization or acidification of the environment, depending on the availability of carbon. Carbon limitation triggered extracellular accumulation of ammonia and alkalinization, whereas an excess of carbon induced acidification through the release of gluconic acid [23]. These findings are of biological relevance because pathogens are likely to encounter different levels of carbon availability, depending on the host niche or the stage of infection (biotrophic or necrotrophic). For example, a postharvest pathogen will be exposed to gradually increasing sugar levels as the fruit ripens and therefore may undergo a switch from alkalinization to acidification during the infection process."

"In contrast to ambient pH, pHi tends to be constant and tightly regulated [34]. Nevertheless, rapid changes in pHi can occur in response to different stimuli, such as shifts in extracellular pH or nutrient status [35]. For example, a rapid and transitory decrease of pHi upon extracellular acidification was detected in an Aspergillus niger strain, expressing the pH-sensitive green fluorescent protein (GFP) variant pHluorin [36]. It is increasingly appreciated that pHi acts as a general regulator of cellular functions, such as growth and proliferation [37], life span [38], and nutrient response [39]. So far, the role of pHi in fungal infection has not been examined in detail, but it is conceivable that it could act as a signal linking extracellular alkalinization to activation of the IG MAPK and pathogenicity (Fig 1)."