Candida Overgrowth. What To Do Now?

[Strongbad]

I had the same thing but with cod liver oil rather than hemp, it may have just been the A & D but I doubt it. It also helped with gut inflammation. I received blood tests back today and definitely have low estrogen so will probably be taking DHEA/Preg in a bit.

I'm still puzzled by the hemp oil recommendation.

1. Omega 6:3 ratios in health animals is closer to 2:1 than 4:1
2. Hemp oil has a lot of linoleic acid which has incredibly harmful metabolites. Maybe hemp oil has enough vitamin E to be ok? If it does the job great but I'm still a skeptic.

I can only vouch hemp oil from my personal anecdote of using it. But scientifically, kineticz can explain it much better than I do.

And yeah, hemp oil has lots of vitamin E.

I believe this should be discussed in this thread instead:
Undermethylators, Ketogenesis [non Peat]

 

[CarbAppreciator]

Im curios if you ever tried aspirin for candida? Also, have your had problems eating high sulphur foods like garlic, onions, eggs, broccoli etc?

 

[Strongbad]

Im curios if you ever tried aspirin for candida? Also, have your had problems eating high sulphur foods like garlic, onions, eggs, broccoli etc?

Yes, I have. I even replied to the original thread here: Aspirin As An Antifungal Drug, Even Against Candida

No, I have no problems with high sulphur foods. As the matter of fact, they're extremely instrumental in killing candida for me. Experienced lots of die-off symptoms after eating them.

The only one I didn't eat much was eggs because eggs contain choline and it interfered with l-carnitine supplement I took. I need l-carnitine to boost my heart, burn free fatty acid (from low-carbing) into energy, detoxify toxins and candida in my blood stream and taking care of constipation issues.

 

[CarbAppreciator]

Interesting about the die off symptoms. I have found information on heavy metals being involved in various infections. Mercury seems to be especially correlated to yeast infections. People with mercury toxicity from amalgams usually react strongly to high thiol (sulphur compound) foods like garlic. I suspect the symptoms stem from the thiols moving the metal around causing oxidative stress.
Peat wrote about iron being involved in infections, so maybe other heavy metals are involved too. I'm working on a thread with some studies on this. Could be one factor in the tetracycline's, or aspirin's, anti cancer effects, as they have been shown to chelate metals.

 

[michael94]

detoxify toxins and candida in my blood stream.

What's the mechanism for l-carintine doing this @kineticz ?

 

[kineticz]

What's the mechanism for l-carintine doing this @kineticz ?

Boost cardiac output and lower free glucose by completely oxidizing fatty acids in mitochondria.

 

[whodathunkit]

Boost cardiac output and lower free glucose by completely oxidizing fatty acids in mitochondria.

Thanks for this! I never really understood why it worked except that it "built and repaired mitochondria". I'm sure I read a better explanation of the mechanism, probably several times, but I have fogbrain pretty badly still even if my physical energy is much, much better.

I started using L-carnitine fumarate about three years ago, and it has been one of the four pillars of my recovery ever since. A very valuable supplement.

Ultimately, however, it wasn't enough. Peat seems to be taking me places now that carnitine and the other supps combined with the diet described in this thread couldn't take me. A missing link, maybe. My recovery stalled even when eating full calorie like Strongbad described, but now seems to be underway again with a more "pure" low fat version of Peat than I tried before. We'll see if it holds.

I will also say that I didn't tolerate Peat well before the l-carnitine and other stuff. Not sure I could have gotten to the place where sugar-based oxidative metabolism worked for me without the carnitine.

 

[Amazoniac]

The powerful bromelain enzyme also helps for lysing Candida hyphae, of which I think I had residual amounts from eating a bit of cooked starch and linoleic acid a few weeks ago. I'm better now, and I do believe that pineapple is the best fruit for Candida detox (like most Americans, I was given a few rounds of antibiotics as a teenager). Candida species also actually produce prostaglandin E₂, which acts to transform it into the hyphal form. This has been shown in numerous studies, and it's transformation can be blocked by cyclooxygenase inhibitors. It had also been shown that no other prostaglandin can do this, will all other eicosanoids having negligible effect besides prostaglandin F₂α (with about ¹⁄₃ the activity as prostaglandin E₂). So besides some forms of starch (in my opinion), linoleic acid is also a Candida growth factor (this being indisputable). This gives us yet another reason to avoid linoleic acid.

Interesting post.
What made you think that?

--
Blood Lipids and Infectious Disease, Part II - Perfect Health Diet | Perfect Health Diet

HDL may promote fungal infections. A recent study found that infusion of reconstituted HDL enhances the growth of Candida (25).

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).

OxLDL also loses its normal anti-infective role against Candida. Worse, it inhibits production of antibodies against Candida albicans (63), thus actually hurting anti-fungal immunity.

Candida is an unusual pathogen that is unusually well-adapted to living in the human body. It has learned to turn an important part of human immune defense to its own advantage.

He commented elsewhere that this reflects in blood tests. One of the reasons for low lipids can be fungal infections.
Rayzord mentioned that they're attracted to estrogen, I have no idea what it means, but I know that copper deficiency lowers lipids in a similar negative way. Is there a connection?

I just want to let you know that I respect you regardless of your current microbiota.

 

[Travis]

Interesting post.
What made you think that?

--
Blood Lipids and Infectious Disease, Part II - Perfect Health Diet | Perfect Health Diet

He commented elsewhere that this reflects in blood tests. One of the reasons for low lipids can be fungal infections.
Rayzord mentioned that they're attracted to estrogen, I have no idea what it means, but I know that copper deficiency lowers lipids in a similar negative way. Is there a connection?

There is. You should read the studies on prostaglandin E₂ and Candida. Even in the absence of an exogenous source, Candida albicans will produce its own prostaglandin E₂. This appears obligatory for the species, and it's used as a hormone. In a panel of eicosanoids, only prostanglandins E₂ and F₂α could induce the yeast➝hyphal transition and proliferation; prostaglandin E₂ was the most powerful eicosanoid tested for doing this, by far.

We all have Candida albicans in it's yeast form; predisposing factors for transformation are antibiotics, linoleic acid, and refined carbohydrates (starch > sucrose).

Although bromelain has it's own anti-Candida effect, it's the pineapple chitinases which are more powerful. Yeast and fungi are unique among microbes in having chitin constituting its cell wall. In yeast form, the germ tube is formed which projects from the cell wall and into this projection the entire nucleus migrates and then splits in two—one half going back to the progenitor cell and the other into the tip, which has the second highest concentration of yeast chitin. While still in yeast form, the tip balloons-out to form a second cell separated by the progenitor cell by a relatively long tube. In the center of this tube is a region composed primarily of chitin, a region in which the yeast form of Candida albicans dissolves with its own endogenous chitinases—effecting total separation.

But in the hyphal form, most of these steps never occur. Instead you see the exploratory tip continuing to grow; this projection can project into old wood, old plant matter, and even into the extracellular space of animals. Nonetheless, the hyphae still have the same chitin-containing segments which can by dissolved at any time by using exogenous chitinase. Vertebrates do not synthesize chitin at all. Nonetheless, humans do have two chitinase enzymes in their body's. One is relatively localized, being found most entirely in the stomach and salivary glands, and the other one—which may surprise you—is found in macrophages and T-cells. In macrophages, it is constitutionally expressed intracellulary ostensibly for the digestion of chitin-containing invaders after engulfation (i.e. yeast, fungi); but in T-cells, B-cells, and natural killer cells, this mammalian chitinase (chitotriosidase) can be induced by a few specific cytokines. It has been observed that rats injected with a chitinase (chitotriosidase) have far better survival rates—when also having hyphal Candida—than those which haven't. The pineapple has three chitinases, two of which have (predictably) been shown to be anti-hyphal (nearly all chitinases should theoretically work).

 

[Dave Clark]

There was a Kansas University study that showed using the herb gymnema sylvestra prevented candida yeast from morphing into the fungal form. How effective that would be I don't know, the study was an in vitro study. However, it could be worth trying, since anybody with real candida issues are usually willing to give anything a try. It might be more effective 'after' the candida is under control, preventing it from going back to a full blown fungal problem.

 

[Amazoniac]

There is. You should read the studies on prostaglandin E₂ and Candida. Even in the absence of an exogenous source, Candida albicans will produce its own prostaglandin E₂. This appears obligatory for the species, and it's used as a hormone. In a panel of eicosanoids, only prostanglandins E₂ and F₂α could induce the yeast➝hyphal transition and proliferation; prostaglandin E₂ was the most powerful eicosanoid tested for doing this, by far.

We all have Candida albicans in it's yeast form; predisposing factors for transformation are antibiotics, linoleic acid, and refined carbohydrates (starch > sucrose).

Although bromelain has it's own anti-Candida effect, it's the pineapple chitinases which are more powerful. Yeast and fungi are unique among microbes in having chitin constituting its cell wall. In yeast form, the germ tube is formed which projects from the cell wall and into this projection the entire nucleus migrates and then splits in two—one half going back to the progenitor cell and the other into the tip, which has the second highest concentration of yeast chitin. While still in yeast form, the tip balloons-out to form a second cell separated by the progenitor cell by a relatively long tube. In the center of this tube is a region composed primarily of chitin, a region in which the yeast form of Candida albicans dissolves with its own endogenous chitinases—effecting total separation.

But in the hyphal form, most of these steps never occur. Instead you see the exploratory tip continuing to grow; this projection can project into old wood, old plant matter, and even into the extracellular space of animals. Nonetheless, the hyphae still have the same chitin-containing segments which can by dissolved at any time by using exogenous chitinase. Vertebrates do not synthesize chitin at all. Nonetheless, humans do have two chitinase enzymes in their body's. One is relatively localized, being found most entirely in the stomach and salivary glands, and the other one—which may surprise you—is found in macrophages and T-cells. In macrophages, it is constitutionally expressed intracellulary ostensibly for the digestion of chitin-containing invaders after engulfation (i.e. yeast, fungi); but in T-cells, B-cells, and natural killer cells, this mammalian chitinase (chitotriosidase) can be induced by a few specific cytokines. It has been observed that rats injected with a chitinase (chitotriosidase) have far better survival rates—when also having hyphal Candida—than those which haven't. The pineapple has three chitinases, two of which have (predictably) been shown to be anti-hyphal (nearly all chitinases should theoretically work).

Great info as always. Sounds like a horror movie script.

Fungal Strategies to Evade the Host Immune Recognition - MDPI

"Both big (70–100 µm in diameter) and small (<2 µm) chitin particles are inert, and do not trigger any immune reaction; while intermediate-sized chitin particles (40–70 µm in diameter) induce a proinflammatory response, triggering the production of TNFDiokine and IL-17, and small fragments (2 to 10 µm) induce an anti-inflammatory response through the mannose receptor, co-localizing with the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and TLR9, leading to IL-10 secretion [36,37]. These findings lead us to speculate that, during the course of infection, and on the assumption that intermediate-sized particles of chitin have been produced during the first stages of the infection, inflammation and destruction of the fungus are induced to promote the elimination of the invading organism, but once the fungus has been killed, the chitin particles found will mostly be small, which will then trigger an anti-inflammatory response through the production of IL-10, mitigating inflammation and therefore avoiding excessive tissue injury [36]. The increment in the chitin content, as a consequence of exposure to sublethal concentrations of caspofungin, has a negative impact on the ability of fungal cells to induce cytokine production [38], indicating that upregulation of these wall components might provide an advantage to fungi seeking to escape from interaction with immune cells."

"Although C. albicans yeasts are rapidly recognized and phagocytized in the bloodstream, once inside the macrophage, production of CO2 inside this immune cell induces the dimorphic switch from yeast to hyphae, which drills, and eventually kills macrophages, a way of subverting the host immune system [100,101]. In addition, the morphological transition from yeast to hypha in C. albicans has negative consequences on the ability of immune cells to produce both pro- and anti-inflammatory cytokines, as the later morphology induces low cytokine levels when compared with yeast cells [102]."

"A noticeable strategy to avoid phagocytosis that some fungal pathogens have acquired is to avoid engulfing by phagocytic cells through volume expansion. This can be achieved by either cell size increase or morphogenesis. This is the case of C. neoformans titan cells, as already mentioned (Figure 3 and Table 2). Other fungi reach the volume increase strategy by a morphotype change, as in the dimorphic fungi Coccidioides immitis and C. posadasii. These fungi are present as hyphae in the environment, but once inside the host they form large rounded-shape spherules that reach up to 120 µm in diameter, too large to be engulfed by macrophages [103]. Similarly, the dimorphic fungi P. brasiliensis and P. lutzii can overcome phagocytosis by regulating morphogenesis. Once conidia or hyphal fragments are inhaled by the host, these fungi undergo transformation into multi-budding yeasts cells, characterized by a large mother cell (up to 30 m in diameter) surrounded by multiple daughter cells presenting different shapes, from round to pear-like forms. The whole multi-budding morphotype can occupy an area that ranges from 75 m2 to over 150 m2, depending on the strain, and is difficult to engulf by macrophages [104]."

"A more recent study has shown that when macrophages are engulfing C. albicans hyphae, the phagocytosis rate is determined by the hypha length: hyphae with a length below 20 µm are phagocytosed at a similar rate as yeasts, while longer hyphae are engulfed at a slower rate [108]. Also, after internalization by macrophages, C. albicans yeast cells undergo filamentation, and germ tubes and hyphae can burst the membrane of the phagocytic cell, killing the immune cells [101]."

"Interestingly, it has been found that even before H2O2 exposure, C. albicans cells already have high levels of catalase, and therefore this detoxification mechanism seems to be of great importance in guarding against oxidative stress in this fungus [112]. The intracellular levels of H2O2 are mainly reduced by glutathione peroxidase, with the production of glutathione disulfide from glutathione. Oxidatively damaged proteins are repaired by both the glutathione system and the thioredoxin system [112]."

"Besides iron sequestration, the most well-studied example of nutritional immunity, the struggle for non-iron transition metals during infection is a subject that has recently received significant attention. Zinc is the second most abundant transition metal in humans, functioning as a protein cofactor and displaying both catalytic and structural roles. It is critically important for proper immune function, but there is evidence suggesting that zinc sequestration by the host during infection is a nutritional immunity strategy to impede microbial growth [32,33]. Citiulo et al. determined that, similarly to the siderophore-mediated iron acquisition, the C. albicans hypha utilizes secreted Pra1 as an extracellular zinc scavenger, a so-called zincophore, and the Zn–Pra1 complex is then bound to the fungal surface by zinc transporter Zrt1. Therefore, Pra1 mediates endothelial damage by scavenging host zinc (Table 1) [199]."

"Copper is a metal ion that functions as a structural and catalytic cofactor for enzymes involved in energy generation, oxygen transport, cellular metabolism, and iron acquisition [200]. Cell surface metalloreductases reduce Cu2+ to Cu1+ in Saccharomyces cerevisiae and then copper is internalized by the high-affinity transporters Crt1 and Crt3 [201–203]. Similar genes for those encoding proteins involved in metal homeostasis in S. cerevisiae and C. albicans were found in the genomes of P. brasiliensis, C. neoformans var. grubii, and C. gattii, suggesting that the mechanisms involved in overcoming ion starvation are conserved in those fungi [196]."

"The classical approach to treat fungal infections is antifungal drugs, which target the plasma membrane, synthesis of ergosterol, or reinforcingitsnotdiokine-1,3-glucan. Although the current therapeutic choices are still adequate for the control of most of the patients affected with a disease caused by fungi, the increment in the number of fungal isolates resistant to one or multiple drugs is a major concern. This has driven the scientific community to look for new therapeutic alternatives to expand the repertoire of antifungal drugs. The search for these new molecules should take into account not only the ability to target cell viability but also the expression of virulence factors and the mechanisms to evade the immune response."​

If the body fails to clear excess estrogen when enough proteid is lacking and yeast is attracted to that excess, are these related?

And how did you find out that starch was feeding Candida?
I would like to let you know that I estimate you regardless if you choose to ignore this last question.

 

[Lucenzo01]

Have you tried Betaine HCL?

 

[Obi-wan]

Ron Gdanski wrote a book called Cancer, cause, cure and Cover-up indicating the fungi connection to cancer. Cancer cells contain chitin. Bacteria can pleomorph into fungi

 

[Travis]

Great info as always. Sounds like a horror movie script.

Fungal Strategies to Evade the Host Immune Recognition - MDPI

"Both big (70–100 µm in diameter) and small (<2 µm) chitin particles are inert, and do not trigger any immune reaction; while intermediate-sized chitin particles (40–70 µm in diameter) induce a proinflammatory response, triggering the production of TNFDiokine and IL-17, and small fragments (2 to 10 µm) induce an anti-inflammatory response through the mannose receptor, co-localizing with the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and TLR9, leading to IL-10 secretion [36,37]. These findings lead us to speculate that, during the course of infection, and on the assumption that intermediate-sized particles of chitin have been produced during the first stages of the infection, inflammation and destruction of the fungus are induced to promote the elimination of the invading organism, but once the fungus has been killed, the chitin particles found will mostly be small, which will then trigger an anti-inflammatory response through the production of IL-10, mitigating inflammation and therefore avoiding excessive tissue injury [36]. The increment in the chitin content, as a consequence of exposure to sublethal concentrations of caspofungin, has a negative impact on the ability of fungal cells to induce cytokine production [38], indicating that upregulation of these wall components might provide an advantage to fungi seeking to escape from interaction with immune cells."

"Although C. albicans yeasts are rapidly recognized and phagocytized in the bloodstream, once inside the macrophage, production of CO2 inside this immune cell induces the dimorphic switch from yeast to hyphae, which drills, and eventually kills macrophages, a way of subverting the host immune system [100,101]. In addition, the morphological transition from yeast to hypha in C. albicans has negative consequences on the ability of immune cells to produce both pro- and anti-inflammatory cytokines, as the later morphology induces low cytokine levels when compared with yeast cells [102]."

"A noticeable strategy to avoid phagocytosis that some fungal pathogens have acquired is to avoid engulfing by phagocytic cells through volume expansion. This can be achieved by either cell size increase or morphogenesis. This is the case of C. neoformans titan cells, as already mentioned (Figure 3 and Table 2). Other fungi reach the volume increase strategy by a morphotype change, as in the dimorphic fungi Coccidioides immitis and C. posadasii. These fungi are present as hyphae in the environment, but once inside the host they form large rounded-shape spherules that reach up to 120 µm in diameter, too large to be engulfed by macrophages [103]. Similarly, the dimorphic fungi P. brasiliensis and P. lutzii can overcome phagocytosis by regulating morphogenesis. Once conidia or hyphal fragments are inhaled by the host, these fungi undergo transformation into multi-budding yeasts cells, characterized by a large mother cell (up to 30 m in diameter) surrounded by multiple daughter cells presenting different shapes, from round to pear-like forms. The whole multi-budding morphotype can occupy an area that ranges from 75 m2 to over 150 m2, depending on the strain, and is difficult to engulf by macrophages [104]."

"A more recent study has shown that when macrophages are engulfing C. albicans hyphae, the phagocytosis rate is determined by the hypha length: hyphae with a length below 20 µm are phagocytosed at a similar rate as yeasts, while longer hyphae are engulfed at a slower rate [108]. Also, after internalization by macrophages, C. albicans yeast cells undergo filamentation, and germ tubes and hyphae can burst the membrane of the phagocytic cell, killing the immune cells [101]."

"Interestingly, it has been found that even before H2O2 exposure, C. albicans cells already have high levels of catalase, and therefore this detoxification mechanism seems to be of great importance in guarding against oxidative stress in this fungus [112]. The intracellular levels of H2O2 are mainly reduced by glutathione peroxidase, with the production of glutathione disulfide from glutathione. Oxidatively damaged proteins are repaired by both the glutathione system and the thioredoxin system [112]."

"Besides iron sequestration, the most well-studied example of nutritional immunity, the struggle for non-iron transition metals during infection is a subject that has recently received significant attention. Zinc is the second most abundant transition metal in humans, functioning as a protein cofactor and displaying both catalytic and structural roles. It is critically important for proper immune function, but there is evidence suggesting that zinc sequestration by the host during infection is a nutritional immunity strategy to impede microbial growth [32,33]. Citiulo et al. determined that, similarly to the siderophore-mediated iron acquisition, the C. albicans hypha utilizes secreted Pra1 as an extracellular zinc scavenger, a so-called zincophore, and the Zn–Pra1 complex is then bound to the fungal surface by zinc transporter Zrt1. Therefore, Pra1 mediates endothelial damage by scavenging host zinc (Table 1) [199]."

"Copper is a metal ion that functions as a structural and catalytic cofactor for enzymes involved in energy generation, oxygen transport, cellular metabolism, and iron acquisition [200]. Cell surface metalloreductases reduce Cu2+ to Cu1+ in Saccharomyces cerevisiae and then copper is internalized by the high-affinity transporters Crt1 and Crt3 [201–203]. Similar genes for those encoding proteins involved in metal homeostasis in S. cerevisiae and C. albicans were found in the genomes of P. brasiliensis, C. neoformans var. grubii, and C. gattii, suggesting that the mechanisms involved in overcoming ion starvation are conserved in those fungi [196]."

"The classical approach to treat fungal infections is antifungal drugs, which target the plasma membrane, synthesis of ergosterol, or reinforcingitsnotdiokine-1,3-glucan. Although the current therapeutic choices are still adequate for the control of most of the patients affected with a disease caused by fungi, the increment in the number of fungal isolates resistant to one or multiple drugs is a major concern. This has driven the scientific community to look for new therapeutic alternatives to expand the repertoire of antifungal drugs. The search for these new molecules should take into account not only the ability to target cell viability but also the expression of virulence factors and the mechanisms to evade the immune response."​

If the body fails to clear excess estrogen when enough proteid is lacking and yeast is attracted to that excess, are these related?

And how did you find out that starch was feeding Candida?

They write about interleukin-17 and interleukin-10, yet no mention of the cytokine GM-CSF and it's ability to stimulate the transcription of chitotriosidase: Our endogenous chitinase enzyme which can degrade chitin, the polysaccharide constituting near-exclusively the exteriors of crustaceans and fungi—entirely absent in all invertebrates (that is, those without fungi):

Interferon-γ cannot do this . . . interleukin-4 certainly can't do this. The cytokine GM-CSF appears to have a partial or total monopoly on the induction of mammalian chitinase (and perhaps even an entire street!—besides of course having the elusive Marvin Gardens).

And I had been reading a bit about this Houdini-like escape from macrophages that Candida albicans is alone capable of; no other Candida species can do this: Candida tropicalis cannot do, Candida glabrata cannot do this, and Candida krusei certainly cannot do this:

[Image A depicts hyphae of Candida albicans piercing the exterior of the same macrophage which had previously engulfed it.]

And how did you find out that starch was feeding Candida?

Why, it's common knowledge that starch is always feeding Candida—and is even somewhat well-known that Candida grows best on potato agar. Specifically, glucosamine induces the yeast➝hyphal transition because it is the monosaccharide which constitutes chitin—a polysaccharide. Candida species can make their own glucosamine enzymatically, using the two substrates glucose and glutamine under the direction of glucosamine-6-phosphate synthase. A can of Red Bull provides only one substrate, the glucose, but potatoes and especially grains will provide both in unusually-high amounts. Most dietary tables, charts, and even the majority of pre-1990 scientific publications do not list glutamine. Often enough, glutamine is actually co-classified with glutamate and even reported as such: This co-classification is sometimes made explicit by using the unusual three-letter amino acid code given as: 'Glx'—with the letter 'x' representing an unknown (but necessarily either a 'u' for glutamate or an 'n' for glutamine). Seed-storage proteins are notoriously rich in glutamine (designated either as 'Gln' in the three-letter system or by 'Q' in the one-letter nomenclature), but you won't find accurate glutamine contents on the more basic amino acid charts. To exemplify the high glutamine content of wheat, just have a look a the α-gliadin protein sequence:

These glutamines are direct precursors for glucosamine, in turn the obligatory constituent unit of cell wall chitin. Straight glucosamine powerfully induces the yeast➝hyphal transition, but its precursors glucose + glutamine would be expected to do likewise. So it's not so much that 'starch feeds candida'—which would be harmless, really, as long as it's in yeast form—but it's that high concentrations of glucose (as a polymer) are often found co-localized with high concentrations of glutamine in what are known as 'starchy foods:' wheat, oats, and potatoes. Candida albicans also has amylases and hence can readily depolymerize starch. Candida albicans is commensal; it's everywhere; the only thing to prevent is the yeast➝hyphal transition most powerfully induced by prostaglandin E₂, glucosamine, or both of the latter's precursors in high concentrations. Now add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars.

 

[Amazoniac]

They write about interleukin-17 and interleukin-10, yet no mention of the cytokine GM-CSF and it's ability to stimulate the transcription of chitotriosidase: Our endogenous chitinase enzyme which can degrade chitin, the polysaccharide constituting near-exclusively the exteriors of crustaceans and fungi—entirely absent in all invertebrates (that is, those without fungi):

View attachment 8751
Interferon-γ cannot do this . . . interleukin-4 certainly can't do this. The cytokine GM-CSF appears to have a partial or total monopoly on the induction of mammalian chitinase (and perhaps even an entire street!—besides of course having the elusive Marvin Gardens).

And I had been reading a bit about this Houdini-like escape from macrophages that Candida albicans is alone capable of; no other Candida species can do this: Candida tropicalis cannot do, Candida glabrata cannot do this, and Candida krusei certainly cannot do this:

View attachment 8752
[Image A depicts hyphae of Candida albicans piercing the exterior of the same macrophage which had previously engulfed it.]


Why, it's common knowledge that starch is always feeding Candida—and is even somewhat well-known that Candida grows best on potato agar. Specifically, glucosamine induces the yeast➝hyphal transition because it is the monosaccharide which constitutes chitin—a polysaccharide. Candida species can make their own glucosamine enzymatically, using the two substrates glucose and glutamine under the direction of glucosamine-6-phosphate synthase. A can of Red Bull provides only one substrate, the glucose, but potatoes and especially grains will provide both in unusually-high amounts. Most dietary tables, charts, and even the majority of pre-1990 scientific publications do not list glutamine. Often enough, glutamine is actually co-classified with glutamate and even reported as such: This co-classification is sometimes made explicit by using the unusual three-letter amino acid code given as: 'Glx'—with the letter 'x' representing an unknown (but necessarily either a 'u' for glutamate or an 'n' for glutamine). Seed-storage proteins are notoriously rich in glutamine (designated either as 'Gln' in the three-letter system or by 'Q' in the one-letter nomenclature), but you won't find accurate glutamine contents on the more basic amino acid charts. To exemplify the high glutamine content of wheat, just have a look a the α-gliadin protein sequence:

View attachment 8753

These glutamines are direct precursors for glucosamine, in turn the obligatory constituent unit of cell wall chitin. Straight glucosamine powerfully induces the yeast➝hyphal transition, but its precursors glucose + glutamine would be expected to do likewise. So it's not so much that 'starch feeds candida'—which would be harmless, really, as long as it's in yeast form—but it's that high concentrations of glucose (as a polymer) are often found co-localized with high concentrations of glutamine in what are known as 'starchy foods:' wheat, oats, and potatoes. Candida albicans also has amylases and hence can readily depolymerize starch. Candida albicans is commensal; it's everywhere; the only thing to prevent is the yeast➝hyphal transition most powerfully induced by prostaglandin E₂, glucosamine, or both of the latter's precursors in high concentrations. Now add linoleic acid to this—the prostaglandin E₂ precursor—and you then have a powerful yeast➝hyphal transducer—more commonly known as potato chips, bread, and granola bars.

The Roles of Biotin in Candida Albicans Physiology - Nur Ras Aini Ahmad Hussin

 

[TNT]

The Roles of Biotin in Candida Albicans Physiology - Nur Ras Aini Ahmad Hussin

I don't understand this study. Are they saying Biotin increases or decreases candida?

 

[Amazoniac]

I don't understand this study. Are they saying Biotin increases or decreases candida?

I don't know how this applies when they're parasiting a host, but they might be capable of robbing biotin. There's the idea that it's difficult to have a biotid deficiency without an antagonist, however this type of infestation can be one explanation. You can't restrict biotin because (as mentioned) they adapt to it, but you can eat a nourishing diet and supplement some through the skin.
They say the same thing about pantothenic acid, that a deficiency is improbable, yet some people still benefit from supplementation.

 

[Amazoniac]

A mineral for Candida albicans? . . A Bloody Mineral!

I have read about many things, but I haven't read about that. Did you know that C. albicans has a Δ¹²-desaturase and also a cyclooxygenase-type enzyme giving it the ability of create prostaglandin E₂ de novo, from glucose, without prior assimilation of any ω−6 fatty acid? In Candida albicans: prostaglandin E₂ serves as a morphogenic factor transforming the yeast into the invasive—and more immunoresistant—mycelial, fungal, and hyphal form. If you were to think that a cyclooxgenase inhibitor would limit Candida transformation, they you'd be right! Aspirin is a powerful antifungal agent:

Alem, M. "Effects of aspirin and other nonsteroidal anti-inflammatory drugs on biofilms and planktonic cells of Candida albicans." Antimicrobial agents and chemotherapy (2004)

Aspirin As An Antifungal Drug, Even Against Candida

And as you know: macrophage-engulfed C. albicans can potentially escape from said immune cell making this process, paradoxically, a pathological process; In the pursuit of destroying a pathogen the macrophage only serves to disseminate it. The killing power of the macrophage is depending on many things, not the least being the plasma arginine concentration. In sepsis: circulating L-arginine—and yes, stereochemistry actually matters here because D-arginine is not an iNOS substrate—can be found ranging from about 40·μM to 50·μM, representing low killing-power (and demonstrating its importance), while its normally found at around 70·μM to 90·μM. However! the maximum macrophage killing-power of C. albicans isn't achieved until an L-arginine concentration of 200·μM is reached. For this reason I do recommend taking 1200·mg of L-arginine in the morning when TNFα is at its cirdadian peak, and hence iNOS is also its circadian peak; this amount expected to raise the plasma L-arginine concentration roughly 50·μM, hopefully killing all macrophage-engulfed pathogens while confounding Candida's attempt at dissemination.

Granger, D. "Specific amino acid (L-arginine) requirement for the microbiostatic activity of murine macrophages." The Journal of clinical investigation (1988)

I didn't know that you now also know what I know.
Georginine in the morning and lysine at night?
This might interest you:
Inhibition of neutrophil killing of Candida albicans pseudohyphae by substances which quench hypochlorous acid and chloramines.

Molybdenum could be important, but so is . . . iron! Besides the cloud of free-radical or otherwise reactive small molecules such as nitrogen dioxide, superoxide, and hypochloric acid [sic], emitted in a pathogen-directed manner by neutrophils, this immune cell also secretes lactoferrin. This is done ostensibly to bind iron and keep it from the invading pathogen, perhaps analogous to how tryptophan pyrrolase limits circulating indoles. If you'd think that iron overload was a risk factor in candidemia, and perhaps even infections of all types, then you would be correct:

Abe, F. "Experimental candidiasis in iron overload." Mycopathologia (1985)

Turmeric is also interesting because it contains a lot of iron and antimicrobial properties at the same of the times, wouldn't you expect that something capable of being inviting and destructive at the same could be an effective approach?

 

[Wagner83]

Turmeric is also interesting because it contains a lot of iron and antimicrobial properties at the same of the times, wouldn't you expect that something capable of being inviting and destructive at the same could be an effective approach?

Antibacterial and Antifungal Properties of Turmeric | NHSJS

 

[Samurai Drive]

I did went very low fat for a while. Then again, I've modified the diet so many times within a year, from all OJ + sugar + milk to eventually very low fat (lots of potatoes) to deplete PUFA then to more balanced diet (meat + vegs + carb).

I do recall that the abdominal pain started sometime in March last year when I started the OJ + sugar + milk diet thing. I never knew what it was and it started very weak so I (mistakenly) brushed it off.

Now, it's a beastly monster inside my intestinal tract. As a matter of fact, last night I had major heart palpitation, body running in adrenaline/cortisol and the flare-up pain on lower right abdomen was unbearable. I lost 3 hours of sleep due to the pain.

There's so much information about whether it's candida or not and all the possible solutions in this thread (and the rest of the internet). Haidut did mention that candida overgrowth happened to people with surpressed immune system, so that might be the culprit of all this mess.

And no, I don't have those white spots inside my mouth (based on the Skally's picture).

Anyway, I'm literally scrapping my diet regimen again. I have to thread it very carefully.

Any updates??