home › The Candida Forum › Candida Questions › Sugar binge after 1 week on diet, antifungals & probiotics. Sugar addicted noob only making it worse › Reply To: Sugar binge after 1 week on diet, antifungals & probiotics. Sugar addicted noob only making it worse
Yes, but if the acquired immune tolerance persist, it will growth back again and again. Also, the antagonistic friendly flora plays a role controlling it too. If the flora isn’t in good shape, there is advantage for candida colonization.
This is a complex syndrome that may have different origins, including genetic, immune defects, immune suppressors, and lack of antagonistic flora.
I understand the theory but generally do not agree with it. For instance I have read one or two studies where a weal was induced after a certain therapy, not immune sensitization shots, were administered. One in particular was from using, if i recall properly, a histamine blocker. The effect as I understand it basically reversed the effect that Il-10 had on Th cell differentiation. So yes, one could say there was induced tolerance, but the tolerance was induced from Il-10. Il-10 doesnt just happen to be around in large numbers under normal conditions of a person with candida. Many other intracellular intruders use Il-10 production/imitation as a means of thwarting the immune system and surviving. Treating the effect of that caused an increased cell mediated response towards candida, and probably any other intracellular pathogen. Which leads me to ask if anyone has ever tested cell mediated immunity using the skin test for other pathogens when a negative response to candida was seen?
Well, there are supplements that helps to correct an unbalanced immune response. In the case of chronic candidiasis, Cimetidine looks the most promising. Have you read studies about it ?? It doesn’t boost cell-mediated immunity only but is a histamine inhibitor too.
Case report: successful treatment with cimetidine and zinc sulphate in chronic mucocutaneous candidiasis.
Polizzi B, Origgi L, Zuccaro G, Matti P, Scorza R.
Institute of Internal Medicine, Infectious Disease and Immunopathology, Univerity of Milan, Italy.
The authors evaluated the clinical efficacy of a treatment with cimetidine and zinc sulphate in a patient with chronic mucocutaneous candidiasis. Cimetidine was given at a dose of 400 mg three times daily; zinc sulphate at a dose of 200 mg daily, then adjusted to maintain blood zinc levels at the upper normal range. This treatment lasted 16 months. An impressive and significant reduction of the infectious events and an increased CD4 (helper/inducer) cell counts were observed. The authors conclude that this combined immunopotentiating treatment is safe and inexpensive to treat immunodeficiency disorders.
[Cell-mediated immune function in NPC patients treated with cimetidine].
[Article in Chinese]
Zeng P, Xiao J, Lei Y.
Third Affiliated Hospital, Hunan Medical University, Changsha.
Cimetidine (CMD), an H2 receptor antagonist, was used in combination with radiation for the treatment of patirnts with nasopharyngeal cancer (NPC). In patients treated with radiotherapy alone, there was an increase in the number of CD4+ T cells and in NK cell activity. In patients received combined treatment of radiation and CMD, in addition, there was a decrease in CD8+ T cells with an increase in CD4/CD8 ratio and an increase in IL-2 production. The NK cell activity was also stronger in the latter group. The results suggest that CMD helps restore cell-mediated immunity in NPC patients radiation treated.
The effect of cimetidine, a histamine H2-receptor antagonist, on the immune system in man was investigated in 11 healthy volunteers. Cimetidine was administered orally in daily doses of 800 mg for a period of 7 days. At the end of the administration period the number of peripheral CD8+ (cytotoxic/suppressor) cells had diminished significantly (P<0.05) along with a corresponding increase in the CD4+ (helper/inducer): CD8+ (cytotoxic/suppressor) cell ratio (P<0.01). Compared with pretreatment values, a significant in vitro blastogenic response to mitogen stimulation with concanavalin A (P<0.005), phytohemagglutinin (P<0.01), and pokeweed mitogen (P<0.05) was observed in lymphocytes of volunteers after cimetidine intake. The cell-mediated hypersensitivity as assessed by skin testing of seven recall antigens was also enhanced significantly (P<0.001). Using Spearman's coefficient of correlation to compare mitogen-stimulation tests and skin tests of delayed hypersensitivity to the CD4+:CD8+ ratio, yielded a positive correlation (r=0.89;r=0.85, respectively). These effects were reversible 96 h after the last cimetidine dose. In contrast, leukocytes, total T lymphocytes (CD2+, CD3+), CD4+ (helper/inducer) cells, natural killer cells (Leu7+), immunoglobulins, and total complement, C3, C4 were unaffected by cimetidine administration.
Cimetidine augments Th1/Th2 dual polarized immune responses to recombinant HBV antigens.
Zhang W, Wang J, Su B, Li R, Ding Z, Kang Y, Wang B.
State Key Laboratories of Agro-biotechnology, College of Biological Science, China Agricultural University, Beijing 100094, China.
Cimetidine (CIM) is a histamine H2 receptor inverse agonist used primarily as an anti-stomach acids drug, but recent studies showed that it may also modulate immune responses. To evaluate its potential usefulness as an adjuvant, we determined its immune modulating effects on subunit immunization using an HBV-derived recombinant protein antigen rHBsAg. CIM activated the PI3K-Akt signaling pathway in DCs. As an adjuvant, it activated immunogenic DCs, deactivated tolerogenic T cells (nTreg), and augmented both Th1- and Th2-polarlized immune responses to rHBsAg. As a result, it enhanced both antibody- and cytotoxic T cell-mediated immune responses. Importantly, in comparison with the FDA-approved human adjuvant alum, CIM is superior in its ability to block IL-10 up-regulation and potentiate Th1/Th2 dual polarization. These results suggest that CIM may be a better adjuvant for therapeutic vaccines against chronic viral infection, such as the HBV infection, where dual polarization should allow more effective elimination of infected host cells.