I needed to disable self-signups because I’ve been getting too many spam-type sign-ups lately. Please contact me directly if you want membership on this forum. Thanks.

Forum Navigation
Please to create posts and topics.

White tounge


I want to give an update. I am 23 days in now and I am confident to say that my white tongue is definately fading away.

It's only a question of a few days or weeks at most now and my tongue will be back to completely normal. It's really fascinating.

Orion, rockarolla and Sussan have reacted to this post.

That really is fascinating yeah!! 😀 Was yours "hairy" as well, as in could you grab it? Either way congratulations on your result and Thank you for updating 😊

does anyone have any explanation to how a coated tounge is related to vit A? I mean she has had this a VERY long time. And she has tried so many different things to get rid of it and now it is just gone.

Maybe the reason is "Vitamin" A was suppressing immune system against candida the whole time:

Modulatory role of vitamin A on the Candida albicans-induced immune response in human monocytes

Moreover, atRA significantly suppressed the expression of Dectin-1, a major fungal pattern recognition receptor, as well as the Dectin-1-dependent cytokine production.

Both RAR-dependent and RAR-independent mechanisms seem to play a role in the atRA-mediated immunomodulation. Our findings open a new direction to elucidate the role of vitamin A on the immune function during fungal infections.
The orchestration of the antifungal response starts with the recognition of the pathogen by immune cells provided with fungal pattern recognition receptors (PRR) [23]. Monocytes express most of the fungal PRRs and have shown to play a particularly important role in the early recognition of the pathogen in invasive candidiasis [23, 24]. Moreover, monocytes are the most effective mononuclear cell-type at killing C. albicans, while their cytokine secretion is important for subsequent innate and adaptive immune activation [23, 25]. However, inflammatory monocytes have also been linked to dysregulated immune responses in invasive candidiasis [22]. Thus, modulation of the immune response in monocytes might be of particular importance for the course of infection.
Among the PRRs expressed on these innate cells, Dectin-1 has shown to play a prominent role in the immune response against C. albicans, not only mediating phagocytosis but also triggering the oxidative burst and the production of several pro-inflammatory cytokines.

Hence, in the present study, we analyzed the immunomodulatory role of vitamin A on the innate immune response against C.albicans with a main focus on the Dectin-1-mediated response. For this purpose, we employed β-1,3-glucan beads which were designed to serve as “fungal-like particles” eliciting a dominant Dectin-1 response [27, 28].

Retinoic acid modulates the cytokine production induced by C. albicans and β-1,3-glucan in human monocytes
We assessed the impact of vitamin A on the immune response to C. albicans by challenging monocytes with UV-killed yeasts in the absence or presence of 1 μM atRA. In a first approach, we analyzed the expression of TNFα, IL6, IL12b and IL10 at transcriptional level by Real-Time qPCR. For accurate normalization purposes, we tested the stability of the housekeeping genes among the experimental conditions using the BestKeeper algorithm [33]. Since both PPIB (standard deviation (SD) of the Ct = 0,48; coefficient of variance (CV) of the Ct = 2,60) and HPRT1 (SD(Ct) = 0,49; CV(Ct) = 2,22) showed a highly stable expression, the geometric mean of both genes was used for further relative expression calculations.

After 5 h of incubation with C. albicans yeasts, we could observe a clear increase in the mRNA expression levels of all four cytokines analyzed (Fig. 1a). However, in the presence of atRA in the cell culture medium, the up-regulation of the pro-inflammatory cytokines was significantly suppressed. As shown in Fig. 1a, the C. albicans-mediated expression of TNFα could be dropped from a 78-fold expression (in the absence of atRA) to a 21-fold expression when atRA was present. In a similar way, we could observe a significant reduction of 83 and 96 % in the gene expression levels of IL6 and IL12b, respectively (Fig. 1a). This modulation by retinoic acid occurs in a dose-dependent manner, and an inhibitory effect of atRA on all three cytokines could already be observed with concentrations as low as 0,01 μM (Suppl. Fig. 1). On the other hand, we could not observe any effect of atRA on the C. albicans-induced IL10 expression (Fig. 1a), even if in the absence of fungal challenge, the addition of atRA led to an up-regulation of this anti-inflammatory cytokine (data not shown).

Comparable results were obtained when the monocytes were stimulated with β-1,3-glucan beads to specifically address the Dectin-1-response (Fig. 1b). As shown in Fig. 1b, the activation of this early fungal-recognition receptor, leading to an up-regulation of all three pro-inflammatory cytokines, was down-regulated by atRA at transcriptional level. In contrast, the expression of the anti-inflammatory cytokine IL10 was rather potentiated by atRA, although not in a statistically significant manner.

To further confirm our findings at protein level, we analyzed the culture supernatants for the presence of TNFα, IL6, IL12 and IL10 after 16 h of stimulation with either C. albicans or β-glucan beads. As shown in Fig. 2, pro-inflammatory cytokine secretion upon fungal stimulation was severely affected by atRA. Co-stimulation with atRA decreased the amount of secreted TNFα, IL6 and IL12 in a significant manner, whereas no effect could be observed on the IL10 release. (Fig. 2a). Similar results were observed when the monocytes were stimulated with the β-glucan beads. In this case, atRA showed an inhibitory effect on the release of all pro-inflammatory cytokines, whereas the secretion of IL10 was rather potentiated (Fig. 2b). These observations resemble the results obtained at transcriptional level and suggest a strong anti-inflammatory role of vitamin A in fungal infections.

Since we could observe an impact of vitamin A on the function of Dectin-1 in terms of the receptor-mediated cytokine production, we next wanted to investigate whether vitamin A had an effect on the expression of this PRR. Under the experimental settings of our stimulation assay, the expression of Dectin-1 was measured at transcriptional level after 5 and 16 h of incubation with C. albicans. At both time points, atRA supplementation led to a decreased expression of Dectin-1 mRNA. Moreover, the inhibitory effect of atRA seemed to increase over time, reaching a fivefold down-regulation of Dectin-1 mRNA after 16 h of incubation with C. albicans (Fig. 3a). Similar down-regulation was also observed when cells were stimulated with atRA alone, in the absence of fungal challenge (Suppl. Fig. 2).
Interestingly, C. albicans itself was also able to slightly dampen the expression of Dectin-1 at transcriptional level (Fig. 3a).
Despite the increasing interest in the immunomodulatory role of vitamin A, no evidence has been reported addressing the impact of vitamin A on the immune response to fungi. In the present study, we have characterized the effect of atRA on the C. albicans-induced immune response in human monocytes. Our results show a strong immunomodulatory role for atRA, leading to a highly significant suppression of the fungi-induced expression of TNFα, IL6 and IL12. This down-regulation could be assessed at both transcriptional and post-translational level.

tim and Ourania have reacted to this post.

When I was doing Ray Peat diet, I had chronic white tongue and my breath smelled bad. Now I don't have white tongue at all and my breath doesn't smell like anything most of the time. This was probably one of the quickest things to improve on the low va diet for me. 

rockarolla has reacted to this post.

White tongue is commonly associated with immune deficiency/insufficiency - happens when one is taking steroids/antibiotics or having some sort of chronic infection inhibiting immune system like lyme, etc.

Also RPD is such a mess with no real scientific basis - I was always wondering why it is constantly hooking so many people.

I suppose it is logical that the mouth, which takes in the vitamin A foods, would be affected!  I think that cleansing the mouth is a good idea.  Various methods have been proposed here including tongue scraping and oil pulling.    And of course there are the usual ideas.   I think my mouth is one of my problem areas, still at this point--although I do see progress.  Think of old people and their mouth problems.    (I think it is typical that you reach saturation in VA in old age.  "getting long in the tooth" is a way to say you are getting old).

rockarolla has reacted to this post.


Nice work, thanks for posting that study.

rockarolla has reacted to this post.

Other forms of immunodeficiency which may cause oral candidiasis include HIV/AIDS,[22] active cancer and treatment, chemotherapy or radiotherapy.
Corticosteroid medications may contribute to the appearance of oral candidiasis, as they cause suppression of immune function either systemically or on a local/mucosal level, depending on the route of administration. Topically administered corticosteroids in the mouth may take the form of mouthwashes, dissolving lozenges or mucosal gels; sometimes being used to treat various forms of stomatitis. Systemic corticosteroids may also result in candidiasis.

TLR signaling is modulated by corticosteroids in a cell type-specific fashion resulting in down-regulation of TLR expression, suppression of pro-inflammatory and up-regulation of anti-inflammatory cytokines. 

Retinol suppresses the activation of Toll-like receptors in MyD88- and STAT1-independent manners
Dysregulation of Toll-like receptor (TLR) activation is well known to be linked to development and aggravation of inflammatory diseases and immune disorders. Retinol is reported to participate in regulation of immune responses. However, it has not been fully understood how retinol regulates TLR activation in macrophages. Our results showed that retinol suppressed the expression of various inflammatory cytokines in bone marrow-derived macrophages stimulated with ligands of TLR2, TLR3, or TLR4. These demonstrate that inhibitory effect of retinol is not limited to a single TLR.

tim has reacted to this post.