- April 1, 2014 at 2:20 am #117543
Lactulose is probably the best Prebiotic known so far to increase LAB in the colon, specially Bifidos count.
Scand J Gastroenterol Suppl. 1997;222:45-8.
Lactulose, lactic acid bacteria, intestinal microecology and mucosal protection.
Salminen S1, Salminen E.
During the fermentation of lactulose, short-chain fatty acids are formed with consequent lowering of the colon pH and modification of the microflora. Lactulose promotes the growth of lactic acid bacteria and bifidobacteria and, more specifically, Lactobacillus acidophilus in the colon. Lactulose and lactulose-containing products fermented with lactic acid bacteria lower colonic pH balancing intestinal microecology and normalizing intestinal transit. In animal studies, lactulose promotes a mainly Gram-positive faecal microflora, but large doses of lactulose may be associated with transient diarrhoea. Our studies indicate that lactulose with lactic acid bacteria effectively relieves constipation in human volunteers. Lactulose with lactic acid bacteria in a fermented diary product can balance and prevent radiotherapy-associated diarrhoea and intestinal side effects. Normalizing the intestinal flora and stabilizing mucosal integrity with lactulose has beneficial effects in intestinal disorders. Lactulose and lactic acid bacteria offer a promising ingredient combination for future functional and special dietary foods in treating intestinal disturbances.
A Human Volunteer Study to Determine the Prebiotic Effects of Lactulose Powder on Human Colonic Microbiota
2002, Vol. 14, No. 3 , Pages 165-173 (doi:10.1080/089106002320644357)
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Kieran M. Tuohy, Cherie J. Ziemer, Annett Klinder, Yvonne Knöbel, Beatrice L. Pool-Zobel and Glenn R. Gibson
The prebiotic effects of lactulose were monitored in a human feeding study. Prebiotics are dietary carbohydrates that have a selective microbial metabolism in the gut, directed towards bacteria seen as beneficial, examples being bifidobacteria and/or lactobacilli. The study was conducted in a double blind, placebo controlled manner. A dose of 10 g per day, half the pharmacological dose, was fed to 10 healthy adult volunteers. In parallel, 10 persons were fed a placebo (glucose/lactose). Both culture based methodologies and genetic probing, based around fluorescent in situ hybridization were used to determine bacterial populations. Faecal water genotoxicity was assessed using the Comet assay to investigate the ability of lactulose to protect against DNA damage. Bifidobacteria showed a statistically significant increase during lactulose intake, whilst genetic probing showed a concomitant decrease in clostridia. Viable plate counts of lactobacilli increased when lactulose was fed, but this was not replicated by the genetic probing. During the trial, none of the recruits experienced any significant adverse gastrointestinal symptoms. Single-cell gel electrophoresis, used to assess faecal water genotoxicity, did not reveal that lactulose intervention reduced genotoxicity. The prebiotic nature of 10 g/day lactulose towards the human gut microbiota has been clearly demonstrated in this study. Lactulose is shown to be an effective food-grade prebiotic for healthy adults particularly in sections of the community with low bifidobacterial populations. The value of the more direct, culture independent FISH technique in the microbial ecology of the gut has been demonstrated in this study.
Mycological aspects of gastrointestinal microflora.
Bernhardt H1, Knoke M.
There are two aspects about the presence of Candida in the human orointestinal tract: (i) it is a part of normal human flora and (ii) it is a risk factor for immunocompromised patients. The orointestinal tract can be considered a reservoir for Candida species, several of which are from the oral cavity, stomach, duodenal juice and faeces. Their germ counts in normal small and large bowel do not exceed 10(4) cfu/ml resp.g. The input of Candida to a well-developed faecal flora system under continuous flow culture conditions did not lead to a multiplication of the yeast. The take in of faecal flora into a Candida continuous flow culture diminish Candida germ counts. If, however, the faecal flora was destroyed, e.g. by antibiotics, we found the yeasts multiplying, with the formation of germ tubes and mycelial structures. Colonization by Candida has to be seen as a starting-point of the development of subsequent candidosis in immunosuppressed or intensive care patients. The best protection against Candida colonization in the gut is the existence of a normal bacterial flora. Lactulose, which promotes the Gram-positive potential of faecal flora, may protect indirectly by supporting the indigenous flora.April 1, 2014 at 3:26 am #117548
Tdog333MemberTopics: 25Replies: 245
Look into resistant starch jorge, pretty interesting stuff.April 2, 2014 at 1:15 am #117580April 2, 2014 at 1:55 am #117582
Candida Albicans wasn’t detected.
Abstract: It is known that lactic acid bacteria preparations suppress the intestinal putrefaction and improves defecation, and that lactulose acidifies the intestinal contents and stimulates the proliferationof lactic acid bacteria in the intestines and further inhibits the absorption of ammonia from the intestine, resulting in the decrease in the synthesis of urea in the liver. For this clinical study, 15 patients receiving maintenance hemodialysis were selected and were divided into two groups. They received orally either lactic acid bacteria preparations or lactulose earlier for 6 weeks, followed by administration of their combination for 6 weeks. We examined the effects of each administration on the changes in peripheral blood counts, blood chemistries, intestinal bacterial flora in a lower portion of the rectum and bowel habits. Administration of lactulose combined with lactic acid bacteria preparations following the intake of lactulose alone induced a significant decrease in the serum triglyceride levels and a significant increase in serum phosphate levels. However, administration of lactic acid bacteria preparations in combination with lactulose following the intake of lactic acid bacteria preparations alone induced no significant changes. Plasma levels of ammonia and glycohemoglobin remained unchanged. Administration of lactic acid bacteria preparation and lactulose and their combination induced the increase in the percentages of Streptococcus, Enterococcus and Staphylococcus groups in the lower portion of the rectum, whereas Candida albicans was not detected. The improvement of bowel habits was observed after administration of their combination rather than administration of lactic acid bacteria preparations and lactulose alone. These results suggest that the environmental changes of the intestine produced by administration of lactulose earlier than of the combination with lactic acid bacteria preparations are effective in changing blood chemistries, and that administration of their combination has advantages in improving the bowel habits.April 26, 2014 at 6:38 am #118458
klips32ParticipantTopics: 65Replies: 183
GJ, as always Jorge.
Has anyone tried it on here?April 27, 2014 at 12:40 am #118481
I have mentioned Lactofiltrum and Lactulose in candida forums many times.
I encourage all you to see this study. It is linked to candida albicans growth in the colon and Lactulose effects on it.
It looks like Lactulose doesn’t encourage candida growth.
Textbook of Natural Medicine – Page 972 – Google Books Result
Joseph E. Pizzorno, Michael T. Murray – 2012 – Health & Fitness
Growth In one of the original studies utilizing lactulose to change fecal flora, … also demonstrated the ability of lactulose to inhibit the growth of Candida albicans.
JorgeJune 3, 2014 at 1:30 am #119209
Prebiotic lowered candida colonization according to this study:
Dietary oligofructose and inulin protect mice from enteric and systemic pathogens and tumor inducers.
Buddington KK1, Donahoo JB, Buddington RK.
Prebiotics induce changes in the population and metabolic characteristics of the gastrointestinal bacteria, modulate enteric and systemic immune functions, and provide laboratory rodents with resistance to carcinogens that promote colorectal cancer. There is less known about protection from other challenges. Therefore, mice of the B6C3F1 strain were fed for 6 wk a control diet with 100 g/kg cellulose or one of two experimental diets with the cellulose replaced entirely by the nondigestible oligosaccharides (NDO) oligofructose and inulin. From each diet, 25 mice were challenged by a promoter of colorectal cancer (1,2-dimethylhydrazine), B16F10 tumor cells, the enteric pathogen Candida albicans (enterically), or were infected systemically with Listeria monocytogenes or Salmonella typhimurium. The incidences of aberrant crypt foci in the distal colon after exposure to dimethylhdrazine for mice fed inulin (53%) and oligofructose (54%) were lower than in control mice (76%; P < 0.05), but the fructans did not reduce the incidence of lung tumors after injection of the B16F10 tumor cells. Mice fed the diets with fructans had 50% lower densities of C. albicans in the small intestine (P 80% for control mice), but fewer of the mice fed inulin died (60%; P < 0.05), with mice fed oligofructose again intermediate. The mechanistic basis for the increased resistance provided by dietary NDO was not elucidated, but the findings are consistent with enhanced immune functions in response to changes in the composition and metabolic characteristics of the bacteria resident in the gastrointestinal tract.
See this :
Non-digestible carbohydrates and the intestinal microflora
Compared with the cellulose and wheat fibre groups, a more than 100-fold increase in faecal lactobacilli was observed in rats fed the lactulose diet. These lactic acid bacteria were also stimulated by FOS and resistant starch, though to a lesser extent (fig 3; p<0.05). FOS and especially lactulose increased the number of bifidobacteria (fig 3; p<0.05). Lactulose, FOS, and resistant starch also increased the number of enterobacteria in faeces (fig 3; p<0.05). The levels of these bacterial genera were not affected by S enteritidis infection (data not shown).
View larger version: InJune 4, 2014 at 1:19 am #119241
Ecology of Candida albicans gut colonization: inhibition of Candida adhesion, colonization, and dissemination from the gastrointestinal tract by bacterial antagonism.
Kennedy MJ, Volz PA.
Antibiotic-treated and untreated Syrian hamsters were inoculated intragastrically with Candida albicans to determine whether C. albicans could opportunistically colonize the gastrointestinal tract and disseminate to visceral organs. Antibiotic treatment decreased the total population levels of the indigenous bacterial flora and predisposed hamsters to gastrointestinal overgrowth and subsequent systemic dissemination by C. albicans in 86% of the animals. Both control hamsters not given antibiotics and antibiotic-treated animals reconventionalized with an indigenous microflora showed significantly lower gut populations of C. albicans, and C. albicans organisms were cultured from the visceral organs of 0 and 10% of the animals, respectively. Conversely, non-antibiotic-treated hamsters inoculated repeatedly with C. albicans had high numbers of C. albicans in the gut, and viable C. albicans was recovered from the visceral organs of 53% of the animals. Examination of the mucosal surfaces from test and control animals indicated further that animals which contained a complex indigenous microflora had significantly lower numbers of C. albicans associated with their gut walls than did antibiotic-treated animals. The ability of C. albicans to associate with intestinal mucosal surfaces also was tested by an in vitro adhesion assay. The results indicate that the indigenous microflora reduced the mucosal association of C. albicans by forming a dense layer of bacteria in the mucus gel, out-competing yeast cells for adhesion sites, and producing inhibitor substances (possibly volatile fatty acids, secondary bile acids, or both) that reduced C. albicans adhesion. It is suggested, therefore, that the indigenous intestinal microflora suppresses C. albicans colonization and dissemination from the gut by inhibiting Candida-mucosal association and reducing C. albicans population levels in the gut.
Candida albicans is an opportunistic dimorphic fungus that inhabits various host mucosal sites. Conversion from the yeast to the hyphal form has been associated with increased virulence and mucosal invasiveness. C. albicans morphogenesis is regulated by multiple signals and signaling pathways. However, signals that control morphogenesis in vivo are unknown. We investigated the effects of host long chain fatty acids, eicosanoids, and bacterial short chain fatty acids on control of germination. None of the C18 or C20 fatty acids tested had an effect on enhancing germ tube formation (arachidonic acid, oleic acid, linolenic acid, or γ-linolenic acid). Among the different eicosanoids, both prostaglandin E2 and thromboxane B2 significantly enhanced serum-induced germination by C. albicans. Addition of antiprostaglandin or antithromboxane antibodies to serum alone inhibited germ tube formation by almost 30%, while control antibody had no effect, indicating that these eicosanoids are major morphogenic factors in the serum. Since these molecules also bind to albumin, this may also explain the hyphal transforming activity in serum that associates with albumin. Interestingly, short chain fatty acids (butyric acid), the product of lactic acid bacteria (LAB), inhibited germination. In addition, LAB culture supernatants as well as live LAB also inhibited C. albicans morphogenesis. Overall, these results indicate that fatty acid metabolites and fatty acid pathways can up-regulate and down-regulate germination in C. albicans.
Candida albicans is a normal member of the gastrointestinal (GI) tract microbiota of healthy humans, but during host immunosuppression or alterations in the bacterial microbiota, C. albicans can disseminate and cause life-threatening illness. The bacterial microbiome of the GI tract, including lactic acid bacteria (LAB), plays a vital role in preventing fungal invasion. However, little is known about the role of C. albicans in shaping the bacterial microbiota during antibiotic recovery. We investigated the fungal burdens in the GI tracts of germfree mice and mice with a disturbed microbiome to demonstrate the role of the microbiota in preventing C. albicans colonization. Histological analysis demonstrated that colonization with C. albicans during antibiotic treatment does not trigger overt inflammation in the murine cecum. Bacterial diversity is reduced long term following cefoperazone treatment, but the presence of C. albicans during antibiotic recovery promoted the recovery of bacterial diversity. Cefoperazone diminishes Bacteroidetes populations long term in the ceca of mice, but the presence of C. albicans during cefoperazone recovery promoted Bacteroidetes population recovery. However, the presence of C. albicans resulted in a long-term reduction in Lactobacillus spp. and promoted Enterococcus faecalis populations. Previous studies have focused on the ability of bacteria to alter C. albicans; this study addresses the ability of C. albicans to alter the bacterial microbiota during nonpathogenic colonization.
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