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Showing posts with label Probiotics. Show all posts
Showing posts with label Probiotics. Show all posts

Thursday, 15 November 2018

Probiotics/Prebiotics – Very good for Some, but no Panacea


This is another post that I had waiting for completion; it is not saying do not use pre/probiotics, it is just saying make sure you know what you are doing.  Plenty of people appear to be wasting their money on ineffective bacteria, some people are making themselves sick, but others get a genuine benefit worth paying for. The is no one-size fits all. Some bacteria are good for some people and bad for others.


It gets more expensive the further you live
from Switzerland, but with the right oral 
bacteria you need a very modest amount.

One of today’s studies shows that spending money on stool tests for bacteria to fine tune a therapy may be a waste of money, unless you do your homework first. 

There is currently a lot written about the role of the gut microbiome on human health. Unfortunately, it tends to get simplified into just good bacteria and bad bacteria.  Advice like “take a good bacteria” is not very useful.

The reality is that some people take a store-bought pre/probiotic bacterium and it does nothing, for some it makes them feel worse and for others it makes them feel better.

It is rather like taking a random drug from the pharmacy and hoping for the best. In the case of autism, it is clear that some people make their child’s life worse with these pills, while sometimes it makes them better.

The idea of custom-made personalized probiotics sounds interesting, but it assumes that the bacteria found in a stool sample is representative of what is living in different parts of your intestines. Unfortunately, a recent study in humans that took samples from different parts along the intestines and compared the result with a non-invasive stool sample, found that the results did not correlate. In other words, drawing too many conclusions from the bacteria found in stool samples is unwise. This challenges the business case for   custom-made personalized probiotics.Modifying bacteria in your body has huge therapeutic potential for some people, but the science is still in its infancy. There are also promising results from fecal transplants (Bacteriotherapy), which is another way to modify the gut microbiome.

“As of 2013, fecal transplantation is currently not routinely performed for indications other than recurrent C. difficile colitis. More research studies are still needed to determine if fecal transplantation should be performed for other clinical indications. Fecal transplantation for other clinical indications should be considered experimental, and performed only as part of a research study where your safety is closely monitored.”
                                                                                             

"Although all of our probiotic-­consuming volunteers showed probiotics in their stool, only some of them showed them in their gut, which is where they need to be," co-author Eran Segal from Weizmann added. "If some people resist and only some people permit them, the benefits of the standard probiotics we all take can't be as universal as we once thought.


A group of scientists in Israel claim foods that are packed with good bacteria - called probiotics - are almost useless.
Their study is among the most detailed analyses of what happens when we consume probiotics.
They are seen as healthy and good for the gut, but the results found they had little or no effect inside the body.
The researchers said probiotics of the future would need tailoring to the needs of each individual.
The team at the Weizmann Institute of Science made their own probiotic cocktail using 11 common good bacteria including strains of Lactobacillus and Bifidobacteria.
It was given to 25 healthy volunteers for a month.
They were then sedated and samples were surgically taken from multiple places in the stomach and small and large intestines.
The researchers were looking to see where bacteria successfully colonised and whether they led to any changes in the activity of the gut.
The results in the journal Cell, showed in half of cases the good bacteria went in the mouth and straight out the other end.

                                                          

Highlights

  • The murine & human gut mucosal microbiome only partially correlates with stool
  • Mice feature an indigenous-microbiome driven colonization resistance to probiotics
  • Humans feature a person-specific gut mucosal colonization resistance to probiotics
  • Probiotic colonization is predictable by pre-treatment microbiome & host features
Empiric probiotics are commonly consumed by healthy individuals as means of life quality improvement and disease prevention. However, evidence of probiotic gut mucosal colonization efficacy remains sparse and controversial. We metagenomically characterized the murine and human mucosal-associated gastrointestinal microbiome and found it to only partially correlate with stool microbiome. A sequential invasive multi-omics measurement at baseline and during consumption of an 11-strain probiotic combination or placebo demonstrated that probiotics remain viable upon gastrointestinal passage. In colonized, but not germ-free mice, probiotics encountered a marked mucosal colonization resistance. In contrast, humans featured person-, region- and strain-specific mucosal colonization patterns, hallmarked by predictive baseline host and microbiome features, but indistinguishable by probiotics presence in stool. Consequently, probiotics induced a transient, individualized impact on mucosal community structure and gut transcriptome. Collectively, empiric probiotics supplementation may be limited in universally and persistently impacting the gut mucosa, meriting development of new personalized probiotic approaches.

In this work, we profiled the homeostatic mucosal, luminal, and fecal microbiome along the entirety of the gastrointestinal tract of mice and humans. We demonstrated that solely relying on stool sampling as a proxy of mucosal GI composition and function may yield limited conclusions.
Our results highlight several important concepts. First, we expand the scope of description of the human microbiome bio-geographical compositional and functional landscape, and indicate that extrapolation from stool microbiome communities to those of specific GI mucosal and luminal niches may lead, in some cases, to inaccurate conclusions. By directly comparing the stool and mucosal presence of 11 probiotic strains of the most commonly used probiotic genera, we conclude that probiotic strain expansion in stool, highlighted by most previous studies to be a sign of probiotics efficacy, cannot distinguish between true probiotic-permissive and resistant individuals, in which probiotics in stool represent a transient ‘‘washout’’ of non-colonizing strains passing throughout the GI lumen without significantly adhering to the host mucosal layer.

Second, the marked and person-specific mucosal colonization resistance to probiotics noted in our study may explain the high variability in probiotics effects on the host or its microbiome noted in previous works. One important feature shown in our studies to play a central role in impacting individualized probiotic mucosal colonization is the indigenous gut microbiome, which may drive the observed person-, strain-, and region-specific colonization resistance patterns to probiotics, as previously suggested. Similarly, we have recently demonstrated that person-specific variations in microbiome composition and function may contribute to the variability in glycemic responses to a variety of foods

Finally, the identified baseline microbial and host factors potentially enabling prediction of a probiotics-permissive or -resistant state merit validation in larger cohorts and call for consideration of a transition from anempiric ‘‘one size fits all’’ probiotics regimen design, to one which is based on the consumer. Such a measurement-based approach would enable integration of person-specific features in tailoring particular probiotics interventions for a particular person at differing clinical contexts.


Probiotics can cause SIBO (small intestine bacterial overgrowth)

In the recent study below, it is suggested that probiotic use can lead to small intestine bacterial overgrowth (SIBO) and the elevated levels of D-lactic acid in blood, then leads to “brain fogginess”. Stopping taking the probiotic (and taking an antibiotic) pretty much solves the problem.



Conclusions
We describe a syndrome of Brain Fogginess (BF), gas and bloating, possibly related to probiotic use, SIBO, and D-lactic acidosis in a cohort without short bowel. Patients with BF exhibited higher prevalence of SIBO and D-lactic acidosis. Symptoms improved with antibiotics and stopping probiotics. Clinicians should recognize and treat this condition.

Bacteria to calibrate the immune system

We saw in earlier posts that the bacteria the fetus and baby are exposed to are used to calibrate the future immune response, which is then pretty much fixed for life. During evolution humans have developed expecting to be exposed to certain bacteria, that today we might regard as just dirt. By living in an ultra-clean environment, we are doing the next generation no favours.

Exposure to bacteria from pets and farmyard animals is very healthy, but only when this is done during pregnancy and shortly thereafter. Once the child’s immune system has been programmed to expect almost no bacteria it is maladapted to cope with future allergens and challenges to the immune system. The result is it over-reacts and produces eczema, asthma, food allergies and many other auto-immune diseases.    

An example showing the benefit of applying knowledge of bacteria

At the risk of digression, here is an example of truly beneficial oral bacteria.

Some years ago, in this blog I reviewed the evidence that drinking beetroot juice boosts exercise endurance and lowers blood pressure.  I was intrigued by this idea, since it is a really simple, healthy and it is easy to measure your blood pressure. Beetroot is rich in nitrates (NO3-) and your body coverts these to nitrites (NO2-) and then later on it uses an enzyme called eNOS (endothelial nitric oxide synthase) to produce nitric oxide in your blood vessels. This dilates them (opens them up) and lets more blood through. This allows endurance cyclists, or marathon runners, to keep going longer and for couch potatoes it lowers their blood pressure. People with vascular conditions like vascular dementia should also benefit from more NO, they may lack the enzyme eNOS if they are elderly. We saw this is my post on Arginine, which suggests that older adults should be taking ALA or NAC, rather than blood pressure reducing meds.

Arginine and its Derivatives in Cognitive Impairment




the progressive impairment in endothelium-dependent vasodilation is caused by a progressive alteration of the L-arginine-NO pathwayOnly in old age (after ≈60 years) does the production of oxidative stress appear, leading to the complete compromise of NO availability.  


For the scientist among you, things are actually much more complex.

Cross-talk Between Nitrate-Nitrite-NO and NO Synthase Pathways in Control of Vascular NO Homeostasis


“Inorganic nitrate and nitrite from endogenous and dietary sources have emerged as alternative substrates for nitric oxide (NO) formation in addition to the classic L-arginine NO synthase (NOS)-dependent pathway. Here, we investigated a potential cross-talk between these two pathways in the regulation of vascular function.”

For the rest of us, basically, we are cheating to improve vascular NO homeostasis. Nitrates are present in other food like spinach and kale, foods many people would avoid, just as would beetroot.

I did an experiment to see if a modest dose (200ml) of beetroot juice would reduce my own blood pressure; it did and by more than a trivial amount. So, I thought I would actually continue with it.

Having now done all my homework I have got the blood pressure benefit from just 80ml of beetroot juice a day, along with an understanding of the bacteria in my mouth that converts the nitrate into nitrite. This means I can reduce my beetroot consumption by more than half to a non-bothersome amount.

Any kind of mouthwash will kill the bacteria needed to make nitrite (NO2-), as will toothpaste. Unless you really want to drink a large glass of beetroot juice every day, you just take 80 ml of beetroot juice and slowly swirl it around in you mouth to react with the bacteria that has been multiplying overnight, before you brush your teeth in the morning.

I finally found a 100% beetroot juice that actually tastes pleasant. It is Swiss and so at least it is consistently the same, unlike the others I tried which ended up being more apple juice than beetroot juice or just tasting vile.

The advantages of an 80ml beetroot juice “mouth rinse”: -

·        Lower systolic blood pressure by about 10 mmHG
·        Lower LDL cholesterol, via the flavonoids
·        The betanin (the red colour) protects against Alzheimer’s in animal models
·        Likely has other (neuro) vascular benefits, perhaps including reducing vascular dementia
                                                                                                                 
The bacteria science, as an example of what you can figure out from publicly available sources: -


Abstract

The salivary glands and oral bacteria play an essential role in the conversion process from nitrate (NO3-) and nitrite (NO2-) to nitric oxide (NO) in the human body. NO is, at present, recognized as a multifarious messenger molecule with important vascular and metabolic functions. Besides the endogenous L-arginine pathway, which is catalysed by complex NO synthases, nitrate in food contributes to the main extrinsic generation of NO through a series of sequential steps (NO3--NO2--NO pathway). Up to 25% of nitrate in circulation is actively taken up by the salivary glands, and as a result, its concentration in saliva can increase 10- to 20-fold. However, the mechanism has not been clearly illustrated until recently, when sialin was identified as an electrogenic 2NO3-/H+ transporter in the plasma membrane of salivary acinar cells. Subsequently, the oral bacterial species located at the posterior part of the tongue reduce nitrate to nitrite, as catalysed by nitrate reductase enzymes. These bacteria use nitrate and nitrite as final electron acceptors in their respiration and meanwhile help the host to convert nitrate to NO as the first step. This review describes the role of salivary glands and oral bacteria in the metabolism of nitrate and in the maintenance of NO homeostasis. The potential therapeutic applications of oral inorganic nitrate and nitrite are also discussed.


The role of salivary glands and oral bacteria in the NO3--NO2--NO pathway. Up to 25% of the circulating nitrate is actively taken up by the salivary glands and concentrated 10- to 20-fold in the saliva to maintain the enterosalivary circulation of NO3--NO2--NO. This key process is mediated by sialin, which is an electrogenic NO3-/H+ transporter in the plasma membrane of salivary acinar cells. When saliva nitrate is secreted into the oral cavity with dietary nitrate—which is reduced to nitrite by the commensal facultative anaerobic bacteria at the posterior aspect of the tongue—some of the nitrite is converted into NO at the stomach. However, most of the remaining nitrate and nitrite are absorbed in the intestine and directly enter the systemic circulation, generating NO in blood and tissues under physiologic hypoxia and playing biological effects.


Role of Oral Bacteria on Nitrate Reduction to Nitrite
Humans, unlike prokaryotes, are believed to lack the enzymatic machinery to reduce nitrate back to nitrite. However, due to the commensal bacteria that reside within the human body, it has been demonstrated that these bacteria can reduce nitrate, thereby providing an alternative source of nitrite. Bacteria are vital in the process of converting nitrate to nitrite—the crucial first step in the NO3--NO2--NO pathway.

Location of Nitrate-Reducing Bacteria in the Mouth
After an oral nitrate loading, gastric NO concentration increases continually. The importance of oral bacteria in gastric NO generation has been clearly illustrated in experiments using germ-free sterile rats, in which gastric NO formation is negligible even after a dietary load of nitrate. The experiment also showed that NO is very low in rats treated topically with an antiseptic mouthwash.
Interestingly, the gastroprotective effects of dietary nitrate, discussed in the section below, virtually disappeared in rats treated with antiseptic mouthwash solutions. The posterior surface of the tongue is responsible for the majority of nitrate reduction, while in the entire oral cavity the nitrate reduction is found to vary widely among individuals. Studies on rats have also shown that nitrate reductase activity occurs on the posterior surface of the tongue and that significantly higher proportions of gram-negative bacteria were found deep within the tongue clefts as compared with the surface.


Composition of Nitrate-Reducing Bacteria

The major nitrate-reducing bacteria can be classified into 2 broad categories—the strict anaerobes (Veillonella atypica and Veillonella dispar) and the facultative anaerobes (Actinomyces odontolyticus and Rothia mucilaginosa;). The facultative anaerobe A. odontolyticus also displays markedly greater ability to reduce nitrate following incubation under anaerobic conditions. However, it is the strict anaerobes (Veillonella spp.) that have been found to be the most prevalent nitrate reducers on the tongue and therefore may be a major contributor to nitrate reduction in the oral cavity. Recently, by using 16S rRNA gene pyrosequencing and whole genome
shotgun sequencing and analysis, scientists have found a higher abundance of Prevotella, Neisseria, and Haemophilus than Actinomyces on the posterior surface of the tongue.

Saliva Nitrate Protecting against Gastric Damage

Nitrate secreted from the salivary glands is found to have an unprecedented function in protecting against stress-induced gastric damage. A water immersion–restraint stress assay in rats shows decreased blood flow in gastric mucosa and induced hemorrhagic erosions after bilateral parotid and submandibular duct ligature. In animals that had received either cardiac ligation or oral treatment with povidone-iodine, a potent bactericidal agent, administration of nitrate failed to increase gastric levels of NO and to inhibit the mucosal injury. NO that is formed close to the gastric mucosa can easily diffuse through the mucosa to the submucosal arterioles, causing vasodilatation and thus increasing gastric mucosal blood flow. This process protects gastric epithelial cells from necrosis. In addition, the decrease of mucosal myeloperoxidase activity and the expression of induced NO synthase with nitrate pretreatment imply that nitrate can reduce tissue inflammation, making this mechanism a possible way of gastric protection. In the absence of a dietary nitrate intake, salivary nitrate originates mainly from NO synthase. Thus, oxidized NO from the endothelium and elsewhere is recycled to regulate gastric mucus homeostasis.


Conclusion

There are some very clever things that can be done by modifying the bacteria in your gut, but if you get it wrong you can very easily make things worse. In some cases, people create a problem where non-existed.

Taking probiotics is not so different to taking drugs, care is needed.

You cannot just produce a general list of good bacteria and bad bacteria. The effects of some bacteria are very specific, and an ever so slightly different variant of one bacterium can do something completely different. Also, what is a good bacterium for one person can be a bad bacterium for the next person.

If you go back to when there was a lot of discussion in this blog about probiotics, this pretty much fits in with the comments. A few people had a good result, some people had a horrific experience and for many there was no effect, except on their wallet.
Many supplements actually contain a relatively tiny number of bacteria and by the time you consume them, you have no idea how many are still alive.

Growing your own bacteria gets around the potency problem, once you have found one that actually gives a benefit.

I do think there is great promise to treat a small number of people by transplanting the microbiome of a healthy person. Only a small number of people are going to need this.

The safest way to “improve” your microbiome is through eating a healthy varied diet, with fruits, vegetables and fiber, which many people resist doing.

Regular exposure to pets and their dust/dirt during pregnancy is on my list of how to minimize future autism. Pets are also calming which should lower oxidative stress and of course dogs make you go for long walks.

For late middle-aged people and older, beetroot juice really is a good intervention and for the really committed add a glass of natural yoghurt with teaspoon of turmeric and high flavanol cocoa (if you can find it), otherwise it is rather expensive Cocoavia from Mars. The yoghurt increases the bioavailability of the turmeric ten times, apparently. 




Wednesday, 2 November 2016

Other interesting Probiotic Bacteria for Cholesterol, Osteoporosis, Diabetes, Eczema, Asthma, Cancer and perhaps some Autism



  
In the next 30 to 50 years I think many common diseases will be, in part, treated by bacteria.  There is already a great deal of research to show that gut bacteria play a key role in both some diseases and the effectiveness of some therapies.

I was surprised to read that the effectiveness of some common existing cancer drugs appears to depend on the presence, or not, of specific gut bacteria.

Many gut bacteria have very specific, but different, effects on the immune system.  There may be no one-size-fits-all options and it is not a case of good bacteria and bad bacteria.  Too much of some “good” bacteria and they becomes “bad” bacteria.

Taking a pragmatic approach you can look at the effects of widely available probiotic bacteria and see if any might have a beneficial effect on a specific person’s autism.

We already saw in the trials that people made following Alli from Switzerland’s revelation about the two L.reuteri bacteria found in Biogaia Gastrus, that what is good for one person might not be effective in the next person.

In my case one of the L.reuteri bacteria in Biogaia Gastrus has a profound positive effect on allergy, and hence autism, while the second bacteria has negative behavioral effects.  Fortunately, the L.reuteri protectis bacteria in Biogaia Gastrus can be purchased separately.

Not surprisingly, companies are patenting the bacteria with research-proven therapeutic effects.  Many supplement companies are using the non-patented bacteria because they are cheaper.  Very often they do not specify exactly which sub-type of bacteria they use and you have no means of knowing whether they change the bacteria over time depending on pricing and availability.

Nonetheless if you skim through the probiotic bacteria research and anecdotal evidence there are some interesting options.
 

First a quick recap

So far in this blog we have seen some particularly interesting individual probiotic bacteria:-

Miyairi 588 from Japan produces butyric acid in the gut.  Butyric acid has been shown to have several interesting effects.  It improves immune health and for this reason is included in animal feed.  It has been shown to improve the integrity of gut to avoid “leaky gut”.  It is an HDAC inhibitor which means it may well have epigenetic effects.  It is an alternative to using butyrate supplements.


 Lactobacillus reuteri 17938 (Lactobacillus reuteri Protectis)

This bacteria is the one we are using and it has potent effects on my son’s summertime allergy that makes his autism much worse.

Lactobacillus reuteri ATCC PTA 6475

This is a potent anti-inflammatory bacteria, but its mode of action does not agree with my son, but it seems to do great things for many others.


Viviomixx and VSL#3

We saw that many people with IBS/IBD and some with autism find these two combination bacteria helpful.  Being a mixture of bacteria means that it may be only certain ingredients that have a helpful effect in a specific person with autism.

Many people with types of IBD/IBS do seem to respond well to the combined bacteria found in Viviomixx and VSL#3.


Some other interesting, commercially available, bacteria

I came across several interesting products. 



Lactobacillus reuteri NCIMB 30242

This bacteria is very well researched and has effects on some of comorbidities that effect some people with autism, such as vitamin D metabolism and calcium homeostasis.

As is often the case the benefits mainly relate to the immune system.  This particular bacteria reduces C-reactive protein (CRP) which is a commonly used marked for inflammation.  It reduces “bad” cholesterol and it has an odd effect on vitamin D making it interesting for people with reduced bone density.

I have no idea if it will help some people with autism, but it is very easy to find out since this patented bacteria is available in several products, targeted at your heart, GI or bones but also lightening your wallet.

Given how quick the L.reuteri protectis showed effect (1 day) I only intend to trial NCIMB 30242 for a few days.


Lactobacillus reuteri NCIMB 30242 research



 Objectives
 The objective of this study was to evaluate the effects of probiotic bile salt hydrolase-active Lactobacillus reuteri NCIMB 30242 on cholesterol lowering, mechanism of action and gastrointestinal (GI) symptomatology in hypercholesterolemic adults.
Methods 127 subjects consumed either L. reuteri NCIMB 30242 or placebo capsules over a 9-week intervention period in a randomized controlled trial.
Results L. reuteri NCIMB 30242 capsules reduced LDL-cholesterol by 11.6% (P=0.001), total cholesterol by 9.1%, 
Conclusions L. reuteri NCIMB 30242 capsules should be considered as an adjunctive therapy for hypercholesterolemia and may be useful for promoting GI health.
  



L. reuteri NCIMB 30242 increased serum 25-hydroxyvitamin D by 14.9 nmol/L, or 25.5%, over the intervention period, which was a significant mean change relative to placebo of 17.1 nmol/L, or 22.4%, respectively (P = .003).

CONCLUSIONS:

To our knowledge, this is the first report of increased circulating 25-hydroxyvitamin D in response to oral probiotic supplementation.

  

Building healthy bones takes guts

  
"We know that inflammation in the gut can cause bone loss, though it's unclear exactly why," said lead author Laura McCabe, a professor in MSU's departments of Physiology and Radiology. "The neat thing we found is that a probiotic can enhance bone density."

In the study, the male mice showed a significant increase in bone density after four weeks of treatment. There was no such effect when the researchers repeated the experiment with female mice, an anomaly they're now investigating.





Lactobacillus Reuteri NCIMB 30350


One reader of this blog is already a fan of Lactobacillus Reuteri NCIMB 30350 which comes from BioAmicus in Canada.

BioAmicus have had feedback from other customers who tried it having read the press reports on Lactobacillus Reuteri and autism.

 They told me:-

“The parents who have seen improvement with BioAmicus Reuteri note eye contact, social activity, language use, as well as improved instruction comprehension.”

They plan to make their own autism clinical trial.

                     https://bioamicus.com/autism-research/



Lactobacillus Johnsonii NCIMB 30351

The next interesting bacteria I came across is Lactobacillus Johnsonii.  There numerous strains.

This bacteria has been shown to be behind why children who live in a house with pet dog are protected from asthma.  Numerous studies like the auto immune disease asthma with increased incidence of autism.

The bacteria is protective against development of another auto immune disease, Type 1 diabetes.

Lactobacillus Johnsonii appears to mediate the effectiveness of some common cancer drugs.

BioAmicus have a Lactobacillus Johnsonii bacteria called NCIMB 30351 usually given to babies.
  
As some readers have already highlighted Lactobacillus bacteria can be used to make all kinds of yoghurt, kefir etc.  So you can grow your own at home to keep the cost down.


Lactobacillus johnsonii research





Early-life exposure to dogs is protective against allergic disease development, and dog ownership is associated with a distinct milieu of house dust microbial exposures. Here, we show that mice exposed to dog-associated house dust are protected against airway allergen challenge. These animals exhibit reduced Th2 cytokine production, fewer activated T cells, and a distinct gut microbiome composition, highly enriched for Lactobacillus johnsonii, which itself can confer airway protection when orally supplemented as a single species. This study supports the possibility that host–environment interactions that govern allergic or infectious airway disease may be mediated, at least in part, by the impact of environmental exposures on the gastrointestinal microbiome composition and, by extension, its impact on the host immune response.








  



 Cyclophosphamide is one of several clinically important cancer drugs whose therapeutic efficacy is due in part to their ability to stimulate antitumor immune responses. Studying mouse models, we demonstrate that cyclophosphamide alters the composition of microbiota in the small intestine and induces the translocation of selected species of Gram-positive bacteria into secondary lymphoid organs. There, these bacteria stimulate the generation of a specific subset of “pathogenic” T helper 17 (pTH17) cells and memory TH1 immune responses. Tumor-bearing mice that were germ-free or that had been treated with antibiotics to kill Gram-positive bacteria showed a reduction in pTH17 responses, and their tumors were resistant to cyclophosphamide. Adoptive transfer of pTH17 cells partially restored the antitumor efficacy of cyclophosphamide. These results suggest that the gut microbiota help shape the anticancer immune response.







Although it is known that resident gut flora contribute to immune system function and homeostasis, their role in the progression of the autoimmune disease type 1 diabetes (T1D) is poorly understood. Comparison of stool samples isolated from Bio-Breeding rats, a classic model of T1D, shows that distinct bacterial populations reside in spontaneous Bio-Breeding diabetes-prone (BBDP) and Bio-Breeding diabetes-resistant animals. We have previously shown that the oral transfer of Lactobacillus johnsonii strain N6.2 (LjN6.2) from Bio-Breeding diabetes-resistant to BBDP rodents conferred T1D resistance to BBDP rodents, whereas Lactobacillus reuteri strain TD1 did not. In this study, we show that diabetes resistance in LjN6.2-fed BBDP rodents was correlated to a Th17 cell bias within the mesenteric lymph nodes. The Th17 bias was not observed in the non-gut–draining axillary lymph nodes, suggesting that the Th17 bias was because of immune system interactions with LjN6.2 within the mesenteric lymph node. LjN6.2 interactions with the immune system were observed in the spleens of diabetes-resistant, LjN6.2-fed BBDP rats, as they also possessed a Th17 bias in comparison with control or Lactobacillus reuteri strain TD1–fed rats. Using C57BL/6 mouse in vitro assays, we show that LjN6.2 directly mediated enhanced Th17 differentiation of lymphocytes in the presence of TCR stimulation, which required APCs. Finally, we show that footpad vaccination of NOD mice with LjN6.2-pulsed dendritic cells was sufficient to mediate a Th17 bias in vivo. Together, these data suggest an interesting paradigm whereby T1D induction can be circumvented by gut flora-mediated Th17 differentiation.



  




 Lactobacillus rhamnosus GG

  
This bacteria has numerous scientifically researched beneficial effects. Most recently it was shown to affect the expression of GABA receptors.  For some people with autism this might be beneficial. In particular it may reduce anxiety, since this was the effect noted in mouse research.

Lactobacillus rhamnosus GG (ATCC 53103) is a strain of L. rhamnosus that was isolated in 1983 from the intestinal tract of a healthy human being; filed for patent on 17 April 1985, by Sherwood Gorbach and Barry Goldin, and the 'GG' derives from the first letters of their surnames. 

The patent refers to a strain of "L. acidophilus GG" with American Type Culture Collection (ATCC) accession number 53103; later reclassified as a strain of L. rhamnosus. The patent claims the L. rhamnosus GG (ATCC 53103) strain is acid- and bile-stable, has a great avidity for human intestinal mucosal cells, and produces lactic acid. Since the discovery of the L. rhamnosus GG (ATCC 53103) strain, it has been studied extensively on its various health benefits and currently L. rhamnosus GG (ATCC 53103) strain is the world's most studied probiotic bacterium with more than 800 scientific studies.
The genome sequence of Lactobacillus rhamnosus GG (ATCC 53103) has been decoded.


Medical research and use

While Lactobacillus rhamnosus GG (ATCC 53103) is able to survive the acid and bile of the stomach and intestine, is claimed to colonize the digestive tract, and to balance intestinal microflora, evidence suggests that Lactobacillus rhamnosus is likely a transient inhabitant, and not autochthonous. Regardless, it is considered a probiotic useful for treatment of various maladies, as it works on many levels. Most of the molecular mechanisms are not known, however.

Peanut allergy

Research is showing that L. rhamnosus as a probiotic could stop allergic reactions to peanuts in 80% of children.


Diarrhea

Lactobacillus rhamnosus GG has been shown beneficial in the prevention of rotavirus diarrhea in children. The prevention and treatment of various types of diarrhea has been shown both in children and in adults.


Respiratory tract infections

L. rhamnosus GG may reduce the risk of obtaining respiratory tract infections in children that attend daycare.


Atopic dermatitis, eczema

Lactobacillus rhamnosus GG also has shown potential in treatment and primary prevention of atopic dermatitis, but the results of intervention trials have been mixed. A clinical trial with seven-year follow-up shows L. rhamnosus GG is useful in the prevention of atopic dermatitis in children at high risk of allergy.


Urogenital tract

The clinical health effects of L. rhamnosus GG have been widely studied. Both L. rhamnosus GG and L. rhamnosus GR-1 appear to protect the urogenital tract by excreting biosurfactants to inhibit the adhesion of vaginal and urinary pathogens.


Intestinal tract permeability

L. rhamnosus has been found to reduce intestinal permeability in children who suffer from irritable bowel syndrome, and it also has been found to counter alcohol-related intestinal permeability.

Gastrointestinal carriage of VRE

In 2005, L. rhamnosus GG was first used successfully to treat gastrointestinal carriage of vancomycin-resistant Enterococcus (VRE) in renal patients.

Anxiety

Research published in the Proceedings of the National Academy of Sciences on August 29, 2011 reported this bacterium may have an effect on GABA neurotransmitter receptors. Mice who were fed L. rhamnosus JB-1 had less anxiety and had different levels of a brain-chemical sensor and stress hormones.

This paper was mentioned previously in this blog


There is increasing, but largely indirect, evidence pointing to an effect of commensal gut microbiota on the central nervous system (CNS). However, it is unknown whether lactic acid bacteria such as Lactobacillus rhamnosus could have a direct effect on neurotransmitter receptors in the CNS in normal, healthy animals. GABA is the main CNS inhibitory neurotransmitter and is significantly involved in regulating many physiological and psychological processes. Alterations in central GABA receptor expression are implicated in the pathogenesis of anxiety and depression, which are highly comorbid with functional bowel disorders. In this work, we show that chronic treatment with L. rhamnosus (JB-1) induced region-dependent alterations in GABAB1b mRNA in the brain with increases in cortical regions (cingulate and prelimbic) and concomitant reductions in expression in the hippocampus, amygdala, and locus coeruleus, in comparison with control-fed mice. In addition, L. rhamnosus (JB-1) reduced GABAAα2 mRNA expression in the prefrontal cortex and amygdala, but increased GABAAα2 in the hippocampus. Importantly, L. rhamnosus (JB-1) reduced stress-induced corticosterone and anxiety- and depression-related behavior. Moreover, the neurochemical and behavioral effects were not found in vagotomized mice, identifying the vagus as a major modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain. Together, these findings highlight the important role of bacteria in the bidirectional communication of the gut–brain axis and suggest that certain organisms may prove to be useful therapeutic adjuncts in stress-related disorders such as anxiety and depression.


Weight loss

Research published in the British Journal of Nutrition in 2013 suggests that Lactobacillus rhamnosus CGMCC 1.3724 may increase weight loss in women who are dieting. The research was initiated after several studies showed that the gut bacteria in obese individuals differs significantly from those in thin people. Women in the study lost nearly twice the weight that the placebo group lost. No difference was observed in men, however.

Risks

The use of L. rhamnosus GG for probiotic therapy has been linked with very rare cases of sepsis in certain risk groups, primarily those with a weakened immune system and infants. Ingestion of L. rhamnosus GG is, nevertheless, considered to be safe, and data from Finland show a significant growth in the consumption of L. rhamnosus GG at the population level has not led to an increase in the number of Lactobacillus bacteraemia cases.



Probiotic Lactobacillus Probiotic rhamnosus downregulates FCER1 and HRH4 expressionin human mast cells



Abstract

AIM: To investigate the effects of four probiotic bacteria and their combination on human mast cell gene expression using microarray analysis.
METHODS: Human peripheral-blood-derived mast cells were stimulated with Lactobacillus rhamnosus (L. rhamnosus) GG (LGG®), L. rhamnosus Lc705 (Lc705), Propionibacterium freudenreichii ssp. shermanii JS (PJS) and Bifidobacterium animalis ssp. lactis Bb12 (Bb12) and their combination for 3 or 24 h, and were subjected to global microarray analysis using an Affymetrix GeneChip® Human Genome U133 Plus 2.0 Array. The gene expression differences between unstimulated and bacteria-stimulated samples were further analyzed with GOrilla Gene Enrichment Analysis and Visualization Tool and MeV Multiexperiment Viewer-tool.
RESULTS: LGG and Lc705 were observed to suppress genes that encoded allergy-related high-affinity IgE receptor subunits α and γ (FCER1A and FCER1G, respectively) and histamine H4 receptor. LGG, Lc705 and the combination of four probiotics had the strongest effect on the expression of genes involved in mast cell immune system regulation, and on several genes that encoded proteins with a pro-inflammatory impact, such as interleukin (IL)-8 and tumour necrosis factor alpha. Also genes that encoded proteins with anti-inflammatory functions, such as IL-10, were upregulated.
CONCLUSION: Certain probiotic bacteria might diminish mast cell allergy-related activation by downregulation of the expression of high-affinity IgE and histamine receptor genes, and by inducing a pro-inflammatory response.





Bifidobacterium Infantis 35624 


Bifidobacterium infantis 35624  is marketed in the US by Proctor & Gamble, while in Europe it is sold by the Irish developer.

It is well researched and does have effects beyond the gut.


Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut



Certain therapeutic microbes, including Bifidobacteria infantis (B. infantis) 35624 exert beneficial immunoregulatory effects by mimicking commensal-immune interactions; however, the value of these effects in patients with non-gastrointestinal inflammatory conditions remains unclear. In this study, we assessed the impact of oral administration of B. infantis 35624, for 6‒8 weeks on inflammatory biomarker and plasma cytokine levels in patients with ulcerative colitis (UC) (n = 22), chronic fatigue syndrome (CFS) (n = 48) and psoriasis (n = 26) in three separate randomized, double-blind, placebo-controlled interventions. Additionally, the effect of B. infantis 35624 on immunological biomarkers in healthy subjects (n = 22) was assessed. At baseline, both gastrointestinal (UC) and non-gastrointestinal (CFS and psoriasis) patients had significantly increased plasma levels of C-reactive protein (CRP) and the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) compared with healthy volunteers. B. infantis 35624 feeding resulted in reduced plasma CRP levels in all three inflammatory disorders compared with placebo. Interestingly, plasma TNF-α was reduced in CFS and psoriasis while IL-6 was reduced in UC and CFS. Furthermore, in healthy subjects, LPS-stimulated TNF-α and IL-6 secretion by peripheral blood mononuclear cells (PBMCs) was significantly reduced in the B. infantis 35624-treated groups compared with placebo following eight weeks of feeding. These results demonstrate the ability of this microbe to reduce systemic pro-inflammatory biomarkers in both gastrointestinal and non-gastrointestinal conditions. In conclusion, these data show that the immunomodulatory effects of the microbiota in humans are not limited to the mucosal immune system but extend to the systemic immune system.


The research highlighted by Proctor & Gamble is here:-




The product is sold as Alflorex in Europe and Align in the US.





Conclusion

One big issue with all probiotics is just how potent they are when you actually consume them, rather than when they are manufactured.

Most people are taking probiotics for very general reasons, but people with IBS/IBD are a group who have very specific problems.  VSL#3 and Viviomixx do seem to be the probiotics of choice among those with IBS/IBD.

For allergy and atopic dermatitis some people clearly benefit from specific probiotics such as Bifidobacterium lactis BB-12 and Lactobacillus GG, but not all people respond.

Lowering cholesterol by probiotic is very easy to verify, so I presume it really must work in some cases.

Generally reducing colic, reflux, gas etc. in babies is a claim made for numerous probiotics.

You could spend a vast amount of money on probiotics for autism and it really is only worth using one(s) that have a genuine impact.

It would be useful to collect some data on what dosage is required when somebody actually does respond behaviourally to a probiotic.  Thanks to Alli and other readers I think we have the data on Biogaia products.

So far only one reader has given feedback on Lactobacillus Reuteri NCIMB 30350 (Bioamicus), but it was positive. The people at BioAmicus in Canada are very interested to know if their products are effective in some autism.

There are many people in the US using Culturelle for kids with autism, but I did not see any rave reviews.  Probably it is used for GI problems rather than to improve autism itself.

It does depend a lot where you live, how easy it is to access specific probiotics at a reasonable price.  Some are much cheaper in the US and some cheaper in Europe.


My current list of potentially interesting probiotics is:-





I really never expected to be writing about the merits of probiotics. It was a big surprise to learn that Miyiari 588 is put in animal feed to improve immune health via increasing the SCFA (short chained fatty acid) butyric acid.  Butyric acid is relevant to autism.  It was a bigger surprise to see L.reuteri Protectis reduce my son’s troublesome pollen allergy and changed the colour of his nose.

It is worthwhile doing some experimentation to see what, if anything, actually is helpful.

There are sound reasons why some people with autism may respond to one of the above bacteria.  As of now though, Biogaia is the probiotic of choice to try first, since many people with autism respond well.


All positive and negative feedback on these, or any other probiotic bacteria is very welcome.