Looking at the Body as a Fish Tank

[LymeEnigma]

Joe Ham posted an article at LNE the other day on H. pylori and how it contributes to both benefit and destruction of the host, perhaps acting more like a symboint than a pathogen. Here is the link: www.lymeneteurope.org/forum/viewtopic.php?f=13&t=1678

Here is the direct link to the article: www.economist.com/science/displaystory.cfm?story_id=11959214

So, this got me thinking....

Anyone who has ever kept a fish tank knows about the ammonia/nitrogen cycle that occurs in their "pseudo-ecosystem." A certain amount of nitrifying bacteria need to be present in a tank in order to deal properly with the waste produced by the fish: not enough beneficial bacteria, and the tank will experience an ammonia spike, followed by a spike in nitrates and nitrites, all of which, depending on the levels, can poison the fish and leave them susceptible to disease. For example, you rarely find septicemia, pop-eye, or fin rot in a well-cycled, well-maintained tank, but those diseases are very common in poorly maintained tanks.

So ... what about the "pseudo-ecosystem" that exists within our bodies? We all know that we have our own beneficial bacteria; without them our bodies fall out of homeostasis. I think we need to ask ourselves: how much damage are we really doing to our bodies, when we take long-term antibiotics? We can replace certain ones (Lactobacillus and Bifidobacterium, for example), but what about the ones we don't readily replace? Might I have "asthma" now because I eradicated in me bacteria that was keeping my lungs healthy? Might there be more side effects than we are aware of? Is there a better approach? Do the benefits really outweigh the risks -- in the long run? Should we be attempting to work with the mix of bacteria in our bodies, as opposed to against them?

[LymeEnigma]

A basic explanation of the ammonia/nitrogen cycle in a fish tank: www.thetropicaltank.co.uk/cycling2.htm

[LymeEnigma]

World J Gastroenterol. 2005 Feb 14;11(6):908-11.
Links
Comparison of probiotics and lactulose in the treatment of minimal hepatic encephalopathy in rats.

Jia L, Zhang MH.

Department of Digestive Diseases, Affiliated First People's Municipal Hospital, Guangzhou Medical College, Guangdong, China. [e-mail]

AIM: To compare the efficacy of probiotic preparation Golden Bifid and lactulose on rat experimental model of minimal hepatic encephalopathy (MHE) induced by thioactamide (TAA). METHODS: MHE was induced by intraperitoneal injection of TAA (200 mg/kg) every 24 h for two consecutive days. Thirty-six male MHE models were then randomly divided into 3 groups: TAA group (n = 12) received tap water ad libitum only; lactulose group (n = 12) and probiotics group (n = 12) were gavaged, respectively with 8 mL/kg of lactulose and 1.5 g/kg of probiotic preparation Golden Bifid (highly concentrated combination of probiotic) dissolved in 2 mL of normal saline, once a day for 8 d (from the 5(th) d before the experiment to the 3(rd) d of the experiment). The latency of brainstem auditory evoked potentials (BAEP) I was used as an objective index of MHE. The incidence of MHE, the level of serum endotoxin, ammonia, liver function and histological grade of hepatic injury of rats were examined individually. RESULTS: There were no overt HE and rat deaths in 3 groups. The incidence of MHE, the levels of blood ammonia and endotoxin in TAA group, which were 83.3% (10/12), 168.33+/-15.44 mg/dL and 0.36+/-0.04 EU/mL, respectively, were significantly higher than those in lactulose group, which were 33.3% (4/12), 110.25+/-7.39 mg/dL and 0.19+/-0.02 EU/mL, and probiotics group, which were 33.3% (4/12), 108.58+/-10.24 mg/dL and 0.13+/-0.03 EU/mL respectively (P<0.001). It showed that either probiotics or lactulose could significantly lower the level of hyperammonemia and hyper-endotoxemia, lighten centrolobular necrotic areas as well as inflammatory reaction in the liver of rats, normalize the latency of BAEP, and decrease the incidence of MHE. However, no significant differences were observed between these two groups (P>0.05). CONCLUSION: Probiotic compound Golden Bifid is at least as useful as lactulose for the prevention and treatment of MHE. Probiotic therapy may be a safe, natural, well-tolerated therapy appropriate for the long-term treatment of MHE.

PMID: 15682492 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/15682492?ordinalpos=15&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Aliment Pharmacol Ther. 2006 Apr 1;23(7):963-74.

Effect of lactulose and Saccharomyces boulardii administration on the colonic urea-nitrogen metabolism and the bifidobacteria concentration in healthy human subjects.

De Preter V, Vanhoutte T, Huys G, Swings J, Rutgeerts P, Verbeke K.

Department of Gastrointestinal Research, University Hospital Gasthuisberg, KU Leuven, Belgium.

BACKGROUND: Protein fermentation products, especially ammonia, are implicated in the pathogenesis of certain diseases. AIM: To investigate the influence of lactulose and Saccharomyces boulardii cells on the composition of the intestinal microbiota and on the metabolic fate of ammonia by means of lactose-[(15)N, (15)N]-ureide. METHODS: An at random, placebo-controlled, crossover study was performed in 43 healthy volunteers to evaluate the influence of lactulose and/or S. boulardii cells either administered as a single dose or after a 4-week intake period. Urine and faeces were collected. All samples were analysed for (15)N-content by combustion-isotope ratio mass spectrometry. Real-time polymerase chain reaction was applied to determine the composition of the predominant faecal microbiota. RESULTS: A single administration of lactulose significantly decreased urinary (15)N-excretion in a dose-dependent way. After long-term administration of lactulose, a significant reduction of the urinary (15)N-excretion was observed, which was accompanied with a significant increase in the faecal (15)N-output, more specifically more (15)N was found in the bacterial fraction. A significant rise in the Bifidobacterium population was found after lactulose intake. No significant effects were observed after S. boulardii intake. CONCLUSION: Dietary addition of lactulose can exert a bifidogenic effect accompanied by a favourable effect on the colonic NH(3)-metabolism.

PMID: 16573799 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/16573799?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Eur J Gastroenterol Hepatol. 2008 Jun;20(6):506-11.

An open-label randomized controlled trial of lactulose and probiotics in the treatment of minimal hepatic encephalopathy.

Sharma P, Sharma BC, Puri V, Sarin SK.

Departments of aGastroenterology bNeurology, G.B. Pant Hospital, New Delhi, India.

BACKGROUND AND AIM: Minimal hepatic encephalopathy (MHE) is associated with poor quality of life and increased work disability. Treatment with lactulose and probiotics has shown some benefit. We compared lactulose with probiotics and a combination of lactulose plus probiotics in the treatment of MHE. PATIENTS AND METHODS: One hundred and ninety cirrhotic patients without overt encephalopathy [Child's A grade 71 patients (37.4%), Child's B grade 72 patients (37.9%), Child's C grade 47 patients (24.7%)] were evaluated by psychometry (number connection tests A and B or figure connection tests A and B) and P300 auditory event-related potential (P300ERP). MHE was diagnosed by abnormal psychometry and/or P300ERP. Patients were randomized to receive lactulose [group A (n=35): dose 30-60 ml/day], probiotics [group B (n=35): dose 1 capsule three times/day, each capsule contained Streptococcus faecalis 60 million, Clostridium butyricum 4 million, Bacillus mesentricus 2 million, lactic acid bacillus 100 million] and lactulose plus probiotics [group C (n=35)] for 1 month. Response was defined by normalization of the abnormal test parameters. RESULTS: MHE was diagnosed in 105 (55.2%) patients. Of the 105 patients, 75 (71%) had both abnormal psychometry and P300ERP, whereas 90 (86%) had abnormal psychometry alone, and 89 patients (85%) had abnormal P300ERP alone. Significant improvement was seen in abnormal psychometry tests (group A: n=31 vs. n=12, group B: n=29 vs. n=14, group C: n=30 vs. n=10), P300ERP (group A: 376.8+/-22.3 vs. 344.3+/-30.6 ms, group B: 385.4+/-28.5 vs. 355.5+/-27.9 ms, group C: 387.7+/-27.5 vs. 347.7+/-31.5 ms) and venous ammonia levels (group A: 102.3+/-63.1 vs. 69.3+/-33.3 micromol/l, group B: 108.2+/-37.5 vs. 75.7+/-33.0 micromol/l, group C: 96.3+/-27.7 vs. 68.7+/-28.4 micromol/l) in lactulose, probiotics and a combination of lactulose plus probiotics groups after treatment. Normalization of abnormal psychometry and P300ERP was seen in 54.8, 51.6 and 56.6% of patients treated with lactulose, probiotics and lactulose plus probiotics groups, respectively. CONCLUSION: A total of 55% of the patients with cirrhosis had MHE. Lactulose or probiotics or combinations of both are equally effective in the treatment of MHE.

PMID: 18467909 [PubMed - in process]
www.ncbi.nlm.nih.gov/pubmed/18467909?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Curr Pharm Des. 2008;14(14):1376-81.

Genomics can advance the potential for probiotic cultures to improve liver and overall health.

O'Sullivan DJ.

Department of Food Science and Nutrition, Center for Microbial and Plant Genomics, Cargill Building for Microbial and Plant Genomics, St Paul, Minnesota 55108, USA. [e-mail]

The concept of probiotics has evolved immensely since it was first proposed a century ago. There are numerous potential health benefits attributed to certain probiotic bacteria, from preventing gastrointestinal (GI) infections to stimulating the immune system. Recent evidence is now quite compelling for a role of probiotics in enhancing liver health. Liver injury is on the rise worldwide with non-alcohol fatty liver disease (NAFLD) the fastest rising liver problem, due largely to the rise in obesity and type II diabetes. A damaged liver can progress to more serious conditions such as steatohepatitis and cirrhosis, and the intestinal microflora are believed to play a large role in this progression. When the intestinal microbial flora is high in facultative microbes, particularly the Enterobacteriaceae, and low in anaerobes such as bifidobacteria, higher levels of ammonia, endotoxins and other compounds enter the blood stream. This results in direct liver damage and also indirectly from pro-inflammatory cytokines such as TNF-alpha. Probiotics have been shown to modulate the intestinal microflora and decrease the urease producing gram negatives and increase the anaerobic population. While results have been obtained with current probiotic strains, more effective strains could be obtained if all the characteristics bacteria use to survive and compete successfully in the intestine were known. The genomics era is now providing the tools to more effectively understand probiotic interactions in the intestine. This will lead to a new generation of exciting probiotics in the future.

PMID: 18537660 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/18537660?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Hepatology. 2008 Jun 9. [Epub ahead of print]

Control of acute, chronic, and constitutive hyperammonemia by wild-type and genetically engineered Lactobacillus plantarum in rodents.

Nicaise C, Prozzi D, Viaene E, Moreno C, Gustot T, Quertinmont E, Demetter P, Suain V, Goffin P, Devière J, Hols P.

Laboratory of Experimental Gastroenterology, Université Libre de Bruxelles, Brussels, Belgium.

Hyperammonemia is a common complication of acute and chronic liver diseases. Often accompanied with side effects, therapeutic interventions such as antibiotics or lactulose are generally targeted to decrease the intestinal production and absorption of ammonia. In this study, we aimed to modulate hyperammonemia in three rodent models by administration of wild-type Lactobacillus plantarum, a genetically engineered ammonia hyperconsuming strain, and a strain deficient for the ammonia transporter. Wild-type and metabolically engineered L. plantarum strains were administered in ornithine transcarbamoylase-deficient Sparse-fur mice, a model of constitutive hyperammonemia, in a carbon tetrachloride rat model of chronic liver insufficiency and in a thioacetamide-induced acute liver failure mice model. Constitutive hyperammonemia in Sparse-fur mice and hyperammonemia in a rat model of chronic hepatic insufficiency were efficiently decreased by Lactobacillus administration. In a murine thioacetamide-induced model of acute liver failure, administration of probiotics significantly increased survival and decreased blood and fecal ammonia. The ammonia hyperconsuming strain exhibited a beneficial effect at a lower dose than its wild-type counterpart. Improved survival in the acute liver failure mice model was associated with lower blood ammonia levels but also with a decrease of astrocyte swelling in the brain cortex. Modulation of ammonia was abolished after administration of the strain deficient in the ammonium transporter. Intestinal pH was clearly lowered for all strains and no changes in gut flora were observed. Conclusion: Hyperammonemia in constitutive model or after acute or chronic induced liver failure can be controlled by the administration of L. plantarum with a significant effect on survival. The mechanism involved in this ammonia decrease implicates direct ammonia consumption in the gut. (HEPATOLOGY 2008.).

www3.interscience.wiley.com/journal/119817372/abstract

[cobweb2]

Very interesting concept. Thanks

[LymeEnigma]

My cat is on Lactulose, one of the meds listed in a couple of the articles above; he will likely have to be on it for the rest of his life (he suffers severe constipation and vomiting without it). I have to wonder if, perhaps, he also suffers from gastroparesis ... and if the probiotic properties of the Lactulose might be a clue to treatments of human gastroparesis?

Moreover ... might Kitty have this issue due to a TBI of his own?