Mutaflor

[ecstatichamster]

This is most interesting:
It has been argued that some of the effects of probiotics are caused by cellular components, so that the organisms would not be required to be alive and establish colonization in the gut [54]. Nevertheless, according to Caselli and coworkers, the definitions of probiotics used by the World Health Organization and the Food and Health Organization include that they have to “remain viable and stable after culture, manipulation, and storage before consumption (and) have to survive to gastric acid and biliary and pancreatic digestion” [55]. These authors argue that, since the host’s pattern recognition receptors (PRRs) play a pivoting role in probiotic applications, it would be irrelevant whether the bacteria were dead or alive [55]. If this argument were accepted, one can only wonder why probiotic products are based on living organisms, which are more difficult to produce, store, and quality control than preparations of cellular components. My gut feeling (pun intended) is that living organisms have more effect than dead ones, though there are few data to support one or the other view.

Thanks @Tarmander

 

[ecstatichamster]

Interesting, thanks for sharing. Its actually in line with what nissle himself said ( difficult cases should take 3-4 months )
I have started taking it a few days ago. Cannot yet explain the effects, but there certainly is a reaction...I plan on taking it for a longer time.

And @ecstatichamster funny you mention that. I started freezing after taking it. I am normally never cold , more uncomfortably warm ,but yesterday I was walking around with a friend of mine and i just had to go into a cafe to warm up . Also at home I notice I am more cold.
What's your explanation of that?
It might be lowering of metabolism but I also suspect it lowers blood sugar pretty strong for me ( I get the typicall symptoms) so that might be the explanation . Do you notice any change in weight?

I am almost sure that it has a powerful effect on lowering blood sugar. That is what I experience. I can drink a Coke, and my temps go from 94.5 (!!) to 99, then in the 96s. I am taking T3, and that really accentuates these swings.

It is difficult to keep blood sugar up actually while taking this. Bizarre!

 

[ecstatichamster]

Any thoughts about taking this while taking the ground up well cooked mushrooms?

I’m spreading the mushrooms hours from the EcN, but maybe I should stop the mushrooms for awhile?

 

[Tarmander]

I am almost sure that it has a powerful effect on lowering blood sugar. That is what I experience. I can drink a Coke, and my temps go from 94.5 (!!) to 99, then in the 96s. I am taking T3, and that really accentuates these swings.

It is difficult to keep blood sugar up actually while taking this. Bizarre!

That is fascinating...could interpret that several different ways...good and bad

 

[Tarmander]

Any thoughts about taking this while taking the ground up well cooked mushrooms?

I’m spreading the mushrooms hours from the EcN, but maybe I should stop the mushrooms for awhile?

I am not sure how Mushrooms affect ecoli. I found this list, and am guessing that anything that is "effective" against Ecoli would make Mutaflor less effective:

 

[ecstatichamster]

Thanks! I’ll stick to bamboo shoots for a bit then...and skip the mushrooms.

 

[Mauritio]

I am almost sure that it has a powerful effect on lowering blood sugar. That is what I experience. I can drink a Coke, and my temps go from 94.5 (!!) to 99, then in the 96s. I am taking T3, and that really accentuates these swings.

It is difficult to keep blood sugar up actually while taking this. Bizarre!

Yes that's why I am contemplating going back to 1 capsule per day. I have taken 3 the first day,while the first capsule had wonderfull effects ,after the second I became irritable and couldn't focus.
Dont quite get what you mean. I guess you want to point at the temperature swings and that they're caused by mutaflors effect on blood sugar?! Do your temps normally go up that far ?

Like @Tarmander said it could be that its boosting metabolism or its slowing it down somehow...
I hope for the first, which is supported by my appetite ,which has definitely increased . I have the sameish weight but eat more .
The increased appetite alone makes me happy since I have had a tendency to undereat because of a lack of appetite.

 

[Mauritio]

This study reviews Ecoli probiotics in general:Insights from 100 Years of Research with Probiotic E. Coli

I will also put this quote here for people's reference for all the different studies out there on Mutaflor:


"E. coli Nissle
Most studies in which EcN was applied to treat human illness relate to inflammatory bowel disease (IBD). The oldest published study describing human exposure, from 1989, collected data from 1074 patients with either functional enteric disorders or IBD, who had taken EcN as recorded by their physician [28]. The study reported a tolerance in more than 90% of the patients, with initial side effects not requiring termination in 2.8%, and termination due to adverse reactions in 1.5% of the patients. Of those with functional intestinal disorders, 84% subjectively judged the treatment to be good to very good; for IBD, this was 78%. As already mentioned above, a double-blind placebo-controlled clinical trial confirmed that IBD patients indeed responded to EcN treatment, though significant improvement was only apparent after 10 to 11 weeks of treatment [24]. In this study, patients with altered enteric microbiota (e.g., after gastroenterocolitis or following the intake of antibiotics) responded best. The abovementioned observation that human β-defensins were induced in vitro and detected at 10 to 15-fold increase following EcN treatment [21] could provide a mechanistic explanation of this positive effect.

Ulcerative colitis (UC), a subcategory of IBD in which the lining of the colon is specifically affected, is typically treated with mesalazine. Already in 1997, a randomized double-blind clinical trial involving UC patients compared 12 weeks of EcN treatment with the gold standard of mesalazine treatment, showing similar start and end scores of the clinical activity index as well as similar relapse rates for both treatments [29]. These results were confirmed 2 years later by another research group [30] and again in a larger study by the research group of the 1997 study [31]. UC can lead to colorectal cancer, for which microsatellite instability in the genome is a possible driver. Rather disappointingly, a follow-up study showed that neither EcN nor mesalazine treatment could prevent the formation of such microsatellite instability in UC patients [32]. Effectiveness of EcN similar to mesalazine was also demonstrated in children between 11 and 18 years suffering from UC [33]. When acute distal UC was treated by rectal administration of EcN, it produced mixed results with no effectiveness for the intention-to-treatment population, but efficacy for the per-protocol population, resulting in dose-dependent remission rates [34]. A volunteer study with healthy individuals was performed to assess if mesalazine could be taken together with EcN, which turned out to have no effect on survival of the probiotic in stools [35]. Whether concomitant treatment with both would increase effectiveness for UC treatment has not yet been described.

In contrast to these positive findings, the effect of EcN on UC was questioned by a recent study comparing pretreatment with ciprofloxacin before EcN administration [36]: 78% of patients receiving ciprofloxacin followed by placebo reached remission, compared to 66% of those receiving EcN after ciprofloxacin. Similarly, for the group receiving placebo instead of ciprofloxacin, again those taking EcN showed lower remission than those receiving twice the placebo (54% and 86%, respectively) [36].

Crohn’s disease, another variant of IBD, is related to adherent-invasive E. coli (AIEC) colonization. It is, therefore, not surprising that treatment for this disorder is rarely tested with EcN, as probiotic products not containing E. coli are usually preferred. A meta-analysis compared all available data on probiotic treatment of CD [37] included only one study that compared EcN treatment with placebo. That study showed no statistically significant difference [38]. More recently, in vitro experiments with biopsies from CD patients and healthy controls showed that EcN lacked the capacity to compete with AIEC [39], which makes it unlikely that EcN can be effective to treat CD.

Since bloating is sometimes reported as a side effect of EcN intake, this was investigated in a randomized double-blind study with healthy volunteers [40]. EcN was well tolerated and did not significantly affect abdominal symptoms, stool frequency, or stool consistency; it had no effect on intestinal gas dynamics.

Other enteric disorders were also challenged with EcN treatment. For instance, a randomized double-blind clinical trial involved 70 patients with constipation [41]. After 4 weeks of therapy, their stool frequency had increased significantly compared with controls, confirmed by crossover patients, when verum patients were changed to placebo and vice versa. When liver cirrhosis patients were treated with EcN, they showed improved liver functions (as by Child–Pugh classification) and reduced endotoxin levels though there were no other significant improvements [42, 43] (publication in Czech). These two publications, describing data obtained from the same study, are thus far the only described application of EcN to treat liver disease.

In a prospective open trial, uncomplicated diverticular disease of the colon was treated with antimicrobials and absorbents, followed by EcN for 5 weeks, which prolonged remission time [44]. Another open trial, this time treating collagenous colitis, showed therapeutic benefit when EcN treatment lasted for at least 4 weeks [45].

Babies were also treated with EcN. In a randomized double-blind clinical trial, healthy newborns were given the bacteria during their first 5 days of life [46]. The stools were EcN-positive in >90% of infants for as long as 6 months. A variety of pathogens was shown to be absent or reduced in numbers during the study. The same group performed a randomized double-blind trial on premature infants where an increase in EcN-specific IgA antibodies could be demonstrated [47]. EcN was further shown in a double-blind randomized trial to shorten acute (viral) diarrhea in infants and toddlers with 2.3 days [48]. Finally, to complete the positive findings for various applications, a case was described of Clostridium difficile-negative pseudomembranous colitis following antimicrobial treatment in an adult, who was successfully treated with multiple intestinal lavages, followed by EcN administration [49].

Less successful was an attempt to treat subjects with hay fever (grass pollen-allergic rhinoconjunctivitis). A randomized double-blind clinical trial with 6 months of treatment covering the full exposure season did not show effects on symptoms, pollen-specific humoral IgE or IgA levels, or a skin prick test [50]. Mutaflor was also not able to reduce carriage of multidrug-resistant E. coli in elderly residents of long-term care facilities [51], though, in this study, only two out of 12 treated subjects had detectable EcN in their feces.

This latter observation brings up an interesting question: how well is EcN capable to colonize the human gut? The applied daily dose of Mutaflor is relatively high (see Table 1), and in several of the abovementioned trials, the product was taken for weeks at a time. Colonization of newborn babies was demonstrated, but in those hosts, the gut is still relatively unoccupied [46]. When seven adult volunteers were orally challenged for 1 week, EcN could only be detected in the stools of four of these [52]. The study combining EcN with mesalazine mentioned above reported that, for the control group (not receiving mesalazine), within 2 weeks after secession of EcN administration, the strain could be detected in the stools of only 40% of individuals, dropping to 20% after 9 weeks [35]. These findings demonstrate that EcN is not very efficient to colonize the human gut long-term. Attempts to improve this colonization potential were not identified. In one animal study, the colonization properties of EcN in mice could be enhanced by introduction of a missense mutation in a histidine kinase gene, but this did not improve its capacity to outcompete enterohemorhagic E. coli challenge [53].

It has been argued that some of the effects of probiotics are caused by cellular components, so that the organisms would not be required to be alive and establish colonization in the gut [54]. Nevertheless, according to Caselli and coworkers, the definitions of probiotics used by the World Health Organization and the Food and Health Organization include that they have to “remain viable and stable after culture, manipulation, and storage before consumption (and) have to survive to gastric acid and biliary and pancreatic digestion” [55]. These authors argue that, since the host’s pattern recognition receptors (PRRs) play a pivoting role in probiotic applications, it would be irrelevant whether the bacteria were dead or alive [55]. If this argument were accepted, one can only wonder why probiotic products are based on living organisms, which are more difficult to produce, store, and quality control than preparations of cellular components. My gut feeling (pun intended) is that living organisms have more effect than dead ones, though there are few data to support one or the other view.

Go to:
The origin of E. coli Nissle 1917
The story of the origin of the Nissle 1917 strain has been told many times and even featured in the publications announcing the release of the sequenced EcN genome [56, 57]. According to this story, Alfred Nissle had isolated the strain from the stool of a First World War soldier, who was the only one of his unit not suffering from dysentery. Some citations state that the lucky soldier remained free from “diarrhea” [58] or “shigellosis” [59] while yet others mention his resistance was against typhoid fever. The original publications cited for this information vary, as Nissle was rather productive and many of his papers are still being cited. Some of the citations refer to his earliest publication, from 1916 [60] cited by, among others, Pöhlmann et al. [61], or a work from 1918 [62], cited by authors who elaborately mention that the soldier had been stationed on the Balkan peninsula [63] although this information was never described by Nissle himself. Others cite a 1925 paper [64], cited by Zyrek et al. [65] which is the oldest record in PubMed mentioning the term “Mutaflor” (though, in fact, Nissle introduced the commercial name in a footnote in a publication from 1919 [66], but that publication is not represented in PubMed). His late works are also frequently cited, e.g., a publication from 1959 [67], cited by Verna and Lucak [59] where it is reported that the soldier was protected from shigellosis, or from 1961 [68] (cited in the review article [58]), or even the posthumous publication that appeared in 1966, a year after Nissle’s death, in which the author, aged 90, had looked back at his long career [69] (cited on page 213 by Tannock [70]).

It is heart-warming to see that so many international authors still read original literature in the German language, but the various citations for this information, and the variation in description of what should be a historical consistent story, is a bit suspicious. Moreover, some of these original publications are hard to come by. I was able to retrieve five original publications written by Alfred Nissle to check what exactly he had published on Mutaflor.

His 1916 paper [60] is very informative and deserves to be summarized here in some detail. He described experiments he performed with E. coli (“Koli” as he called them) isolated from stool samples. He cultured these on agar plates (“Endoagarplatten”) and spiked them with a fixed ratio of 2:3 of “Typhusbacillen” (in later experiments, he cultured the mixture in a broth for 6 or 7 h before plating). On the plates, he observed that some, but not all, of the tested E. coli isolates could inhibit or reduce the growth of what we now call Salmonella enterica serovar Typhi. He called this phenomenon “antagonism” and expressed the number of “Typhus” colonies per 100 “Koli”-colonies as the “antagonistic index” of the assessed E. coli isolate. He then compared this index between strains, describing in detail the difficulty in standardizing the test, performed with inclusion of control strains with a proven high or low antagonistic index. At the extremes, he observed that the strongest antagonistic strains were 1350 times better able to inhibit S. Typhi growth than the weakest tested isolates.

Nissle tried to explain the observed differences in antagonism by differences in lactic acid production, but observed there was no correlation, nor was indole production related. He further reported that strongly antagonistic strains not only inhibited S. Typhi but also “Paratyphus-Dysenterie”, “Kruse-Shiga”, “Dysenterie Flexner”, and “Proteus”. These old names refer to Salmonella enterica serovar Paratyphi, Shigella dysenteriae, Shigella flexneri, and either Proteus vulgaris or P. mirabilis (neither of which are strongly pathogenic but that was not known at that time). He was even able to show antagonism between different E. coli strains, by clever use of a strain that was unable to produce gas on a medium containing glucose (“Traubenzucker”, his strain was an atypical non-gas-former, as have subsequently been characterized and described [71]). This indicator strain was defeated by strong antagonistic E. coli strains but not by weakly antagonistic ones. Nissle further showed that the antagonistic property was lost after heating at 60 °C, which we now know is indicative of proteins or peptides. The phenotype he determined was most probably the result of microcins; it is now known that EcN produces microcins MccM and MccH47 [72].

When he compared E. coli strains obtained from 15 fecal samples of healthy individuals, three were very strong, five were strong, four were medium, and three were weakly antagonistic (it is unclear whether these experiments were performed with the indicator E. coli or with Typhus). In contrast, 25 strains from “pathological stools” produced two reasonably strong, five medium, and 18 weak antagonists. From these observations, Nissle concluded that a strong antagonistic E. coli in the gut might protect against enteric diseases.

The three “very strong” antagonistic strains from healthy stool were described in a bit more detail. One was found by chance, but the other two came from selected individuals: Nissle had visited an army hospital (“Verwundeten-Lazarett”) and had specifically selected patients who reported to have never suffered from enteric diseases, even though they had been exposed to acutely infected patients. He identified two such persons (it was not described why they were hospitalized or where they had served) who produced E. coli with an antagonistic index of 100:10 and 100:3, respectively.

Nissle had no means to conserve his strains other than by subculture. He describes that one of his precious strong antagonizers lost its phenotype after 2 years. He was able to protect the other two, one isolated in March 1915 and the other in September of that year (unclear is, whether both of these were the isolates from the soldiers), from that fate by storing them in capsules made of paraffin or wax. To test their positive effect against infections, he first gave these capsules to healthy volunteers and, after proven safety, to diseased patients. The rest of the 1916 publication describes successful treatments of 11 cases. Case 11 suffered from Typhus infection from 25 July till 8 August 1915 and shed high numbers of “Typhusbacillen” since (from 12 September till 17 April 1916) when treatment was started. The person shed low numbers till 28 April. after which Thypus bacteria could no longer be detected in his stool. The treatment consisted of 52 capsules of “Kolireinkultur” administered in 37 days. Nissle described that the person produced the administered high-antagonistic E. coli in his stool 3 weeks after termination of treatmen (at least he was able to isolate a strain with similar antagonistic properties from the stool). Nissle suggested the capsules as treatment for acute intestinal infections and speculated it might even be effective against other infections, giving the example of diphtheria. The 1916 publication demonstrates the extraordinary scientific skills of Nissle. Not only was he a sharp observer, he also designed his experiments under standardized conditions with inclusion of the necessary controls, tested explanatory hypotheses and discarded these based on experimental evidence, developed means to store his biological material, and performed clinical trials avant la lettre.

In his 1918 publication [62], Nissle continued his investigations with the capsules that were from then on commercially produced under the name “Mutaflor,” though it remains unclear whether the E. coli strain used in the product was his isolate from March or September 1915. Who the individual was from whose stool it was isolated, whether it was one of the soldiers, and if so, where he had been stationed is not disclosed by Nissle. What we can deduc from the literature is that the strain was originally isolated in 1915, possibly from a soldier of unknown nationality, who at that time was treated in a German army hospital. The year “1917” that has become part of the name of this strain present in Mutaflor neither refers to the year of isolation, nor to the year the strain was first publicly described."

Interesting, especially its pro liver and anti- endotoxin effect.

 

[ecstatichamster]

Yes that's why I am contemplating going back to 1 capsule per day. I have taken 3 the first day,while the first capsule had wonderfull effects ,after the second I became irritable and couldn't focus.
Dont quite get what you mean. I guess you want to point at the temperature swings and that they're caused by mutaflors effect on blood sugar?! Do your temps normally go up that far ?

Like @Tarmander said it could be that its boosting metabolism or its slowing it down somehow...
I hope for the first, which is supported by my appetite ,which has definitely increased . I have the sameish weight but eat more .
The increased appetite alone makes me happy since I have had a tendency to undereat because of a lack of appetite.

my temps do not swing like this normally. I’ve also experienced a bit of brain fog I attribute to mutaflor

 

[Ingenol]

@ecstatichamster are you in the US? If so, do you mind sharing where you purchase your Mutaflor?

 

[ecstatichamster]

Mutaflor Probiotic 60 Caps 30 Day Supply with E. coli strain Nissle 1917

 

[Tarmander]

E Coli tend to be the most resistant to anti bacterial herbs:
The in vitro antibacterial activity of dietary spice and medicinal herb extracts. - PubMed - NCBI

 

[Mauritio]

E Coli tend to be the most resistant to anti bacterial herbs:
The in vitro antibacterial activity of dietary spice and medicinal herb extracts. - PubMed - NCBI

Let's hope its the nissle 1917 strain ,some of the other e.coli strains we wouldnt want to be too resisting...

 

[Tarmander]

Looking around the net there are other brands of Mutaflor like this:

MutaFlor Probiotics 100 capsules

However it looks like each capsule is at 250 million CFU where as the one from feelgoodnaturally has 25 X 10^9 CFU which would be 25 billion I believe.

Also I was reading this page, which is a good general purpose FAQ: FAQs | Mutaflor

Found this nugget:

"There are other antibiotics including Clindamycin, Erythromycin and Metronidazole, that E. coli Nissle 1917 has a natural resistance to and these can be given together without any damage to Nissle 1917. If you are on any of these antibiotics including treatments for H. pylori infections in the stomach, Mutaflor® complements the therapeutic regime, mediating anti-inflammatory gut activities, moderating bowel movements that can be upset by the antibiotics, and facilitating regrowth of good flora.

Usefully, E. coli Nissle 1917 does not share genetic elements for antibiotic resistance and will not contribute to antibiotic-resistance in the human gut. It is also sensitive to blood components and gets killed very quickly if it gets into the bloodstream from the gut. This unique aspect of Nissle 1917 makes it a safer probiotic option for individuals at risk of being immune-compromised while on antibiotics."

Macrolides, aka Erythromycin, have said to be really useful to people with CFS. This is just another connection that CFS people tend to have low levels of E. Coli and could benefit from Mutaflor.

 

[ecstatichamster]

excellent find, thanks @Tarmander

I'm on maybe day 5 and I'm slowly getting better. This is working for me. I'm aiming to overcome chronic constipation that I acquired from drinking milk (which I still drink). I am still taking a bit of cascara but things are healing down there...

 

[InChristAlone]

excellent find, thanks @Tarmander

I'm on maybe day 5 and I'm slowly getting better. This is working for me. I'm aiming to overcome chronic constipation that I acquired from drinking milk (which I still drink). I am still taking a bit of cascara but things are healing down there...

I wonder why milk causes constipation for so many people? Milk drinking is supposed to help the bowels as per Dr. Kellogg. Plus babies who are exclusively breastfed have very very soft stool, it isn't until they start solids their poop firms up. There must be a component to cows milk that causes it. Maybe too much calcium for adults??

 

[Blossom]

I wonder why milk causes constipation for so many people? Milk drinking is supposed to help the bowels as per Dr. Kellogg. Plus babies who are exclusively breastfed have very very soft stool, it isn't until they start solids their poop firms up. There must be a component to cows milk that causes it. Maybe too much calcium for adults??

Casomorphin??? I think that’s what Travis might say.

 

[Tarmander]

excellent find, thanks @Tarmander

I'm on maybe day 5 and I'm slowly getting better. This is working for me. I'm aiming to overcome chronic constipation that I acquired from drinking milk (which I still drink). I am still taking a bit of cascara but things are healing down there...

That is awesome. Seems like constipation is a big use for it. Keep us updated

 

[Mauritio]

Looking around the net there are other brands of Mutaflor like this:

MutaFlor Probiotics 100 capsules

However it looks like each capsule is at 250 million CFU where as the one from feelgoodnaturally has 25 X 10^9 CFU which would be 25 billion I believe.

Also I was reading this page, which is a good general purpose FAQ: FAQs | Mutaflor

Found this nugget:

"There are other antibiotics including Clindamycin, Erythromycin and Metronidazole, that E. coli Nissle 1917 has a natural resistance to and these can be given together without any damage to Nissle 1917. If you are on any of these antibiotics including treatments for H. pylori infections in the stomach, Mutaflor® complements the therapeutic regime, mediating anti-inflammatory gut activities, moderating bowel movements that can be upset by the antibiotics, and facilitating regrowth of good flora.

Usefully, E. coli Nissle 1917 does not share genetic elements for antibiotic resistance and will not contribute to antibiotic-resistance in the human gut. It is also sensitive to blood components and gets killed very quickly if it gets into the bloodstream from the gut. This unique aspect of Nissle 1917 makes it a safer probiotic option for individuals at risk of being immune-compromised while on antibiotics."

Macrolides, aka Erythromycin, have said to be really useful to people with CFS. This is just another connection that CFS people tend to have low levels of E. Coli and could benefit from Mutaflor.

Great ! Do you happen to know if any of the other antibiotics like the tetracyclines or penicilin have the same effect?

 

[Tarmander]

Great ! Do you happen to know if any of the other antibiotics like the tetracyclines or penicilin have the same effect?

Seems to be similar: