There is a direct link between clogged liver/gallbladder and the spread of candida albicans.
It is very simple: one of the functions of bile (bile acids) is to keep candida albicans in check- when sufficient levels of bile fluid is present candida can't efectively attach itself to the mucosal layer of GI tract and therefore it cannot proliferate.
I believe now that along with Antibiotics
clogged liver/gallbladder (=decreased bile flow) are top two reasons for systemic candidiasis. Sugar
is just helper. Unlucky you if you both, loaded up on antiobiotics and have clagged liver/gallbladder.
Therefore I feel strongly that clearing up our livers and gallbladders using Liver-Flush
protocol along with diet and loading on probiotics is not complimentary but is mandatory in order to get rid of systemic candidiasis successfuly.
To prove my point I enlist the help of pubmed database.
1) Altered Kupffer cell function, as measured by the increased phagocytosis of C. albicans and LPS-induced NO production, and decreased LPS-induced TNFalpha production were observed in all animals with obstructive jaundice regardless of bile salt replacement. CONCLUSION. Kupffer cell function appears to be differentially affected by obstructive jaundice and these altered functions can occur independent of bacterial translocation.
2)Sepsis is a major cause of morbidity and mortality in infants with cholestatic jaundice. This may be attributed to altered host defense mechanisms. Fungal infection frequently occurs in immunocompromised patients. This study evaluates the effect of biliary obstruction on blood clearance and organ localization of radiolabeled viable Candida albicans. Male Sprague-Dawley rats (140 to 150 g) were placed in 2 groups. Group I (n = 30) were sham-operated controls. Group II (n = 90) underwent ligation and division of the distal common bile duct (CDL). At 1, 2, and 3 weeks following CDL, 10(7) cells/mL radiolabeled viable C albicans were injected via the tail vein. The final distribution of the organisms was calculated and expressed as the mean percent of radiolabeled organisms per gram and per total organ. Blood clearance of C albicans was similarly rapid in both groups. However, there was a significant decrease in the trapping of fungi by the rat liver Kupffer cells (20.3% +/- 7.9% v control 42.5% +/- 15%; P greater than .001), and increased pulmonary localization of bacteria 3 weeks following CDL (53.6% +/- 13.2% v control 41.4% +/- 6.4%). The significant decrease in liver trapping and increased lung localization of C albicans in CDL rats, may result in systemic reemergence of fungi and play a role in the susceptibility to fungal infection in jaundiced subjects.
3)In an attempt to clarify the comparative values of serological and microbiological examinations for the early diagnosis of systemic candidiasis, antibodies against Candida albicans, serum mannan, and the D-arabinitol creatinine ratio were investigated in a patient with aortic valve endocarditis associated with carcinoma of the bile duct. Candida precipitins and the antibody titer against Candida cell wall mannan were examined by an immunodiffusion technique and hemagglutination test, respectively. Serum mannan was tested by enzyme-linked immunosorbent assay (ELISA) using the biotin-streptavidin procedure. The upper limit of negativity of the assay was determined by adding 0.06 to the absorbance of pooled serum from healthy laboratory workers. This value was about 0.8 ng/ml with ELISA. The D-arabinitol concentration in serum was examined by an enzymatic fluorometric method. Rising antibody titers against C. albicans, mannan antigenemia, and an elevated D-arabinitol creatinine ratio were first observed between the 11th and 12th hospital days. Blood cultures obtained on 8th, 9th, and 11th hospital days grew C. albicans after 3 to 4 days of incubation. Of 11 serum samples, 5 were positive for mannan, whereas D-arabinitol creatinine ratio was positive in 7 of 9 samples. Blood cultures was the earliest evidence of Candida infections in our cases. However, because of saprophytic nature of Candida species, tests for antibodies, antigenemia, and the D-arabinitol creatinine ratio in combination with blood cultures are necessary to confirm systemic candidiasis at an early stage of infection.
certain unknown chemical substance(s) produced in the GI
tract of untreated animals, probably by metabolic activities
of those organisms which predominate in the gut, appeared
to inhibit the ability of C. albicans to associate with intestinal
mucosal surfaces. In an attempt to identify such factors,
VFA and secondary bile acids were tested in the mucosal
association assay. It was found that both of these types of
substances reduced the ability of C. albicans to associate
with intestinal mucosal tissues (assays 7 and 8).
5)The liver is affected in up 50 to 75% of compromised hosts with disseminated Candida albicans infection who come to autopsy. The antemortem diagnosis of hepatic candidiasis is rarely made. Blood cultures are negative in approximately 50% of cases, and biochemical parameters of hepatic injury may be of nonspecific value. Additionally, the more commonly seen renal, cardiac, and respiratory involvement may overshadow the hepatic lesion. In a review of 17 autopsy series of disseminated candidiasis, 92 cases with hepatic involvement were identified for a mean prevalence of 13.7%. Hepatic granulomas and microabscesses were the two most common histological lesions attributable to Candida. Inflammatory aggregates, centrilobular congestion, bile stasis, and fatty change were seen less frequently. The diagnosis should be suspected in any compromised host with unexplained fever with or without elevated alkaline phosphatase or bilirubin levels. The diagnosis can be made by percutaneous needle biopsy or at laparoscopy in a majority of cases. Early treatment with Amphotericin is associated with prolonged survival.