270 replies to this topic

[Oakman]

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You can sign up for free, they'll send a poop kit, and return result, plus scientists that need samples for research can buy from them (~80 per your sample), you get a 10% commission.

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Do Gut Microbes Predict or Cause Diseases like Parkinson's? | Martha Carlin | TEDxBoulder

 

 

 

[Nate-2004]

Why is the focus always on Parkinsons when Essential Tremor is far more common by millions? 

 

Anyway, I signed up. Maybe they'll be able to link it to Essential Tremor as well.

[Darryl]

OT: Nate-2004, you may be interested interested in the connection between chronic exposure to the β-carboline harmane and essential tremor. 

 

Laviță et al, 2016. The role of β-carboline alkaloids in the pathogenesis of essential tremor. The Cerebellum, 15(3), pp.276-284.

Epidemiological studies have suggested that neurotoxic agents, especially β-carboline alkaloids (βCAs), might be generated through Maillard-type reaction. βCAs are molecules which are members of a large group of heterocyclic amines (HCAs, the so-called products of cooking meat). βCAs are highly tremorogenic in animals, producing a marked generalized action tremor soon after systemic administration in a wide range of laboratory animals such as mice, rats and monkeys. Administration of βCAs remains currently the main experimental model of ET. 

 

Louis et al, 2007. Blood harmane is correlated with cerebellar metabolism in essential tremor A pilot study. Neurology, 69(6), pp.515-520.

Log blood harmane concentration was a predictor of cerebellar N-acetylaspartate/total creatine; every 1 g^-10/mL unit increase in log blood harmane concentration was associated with a 0.41 unit decrease in cerebellar NAA/tCR.

 

Louis et al, 2008. Dietary epidemiology of essential tremor: meat consumption and meat cooking practices. Neuroepidemiology, 30(3), pp.161-166.

Male cases had higher odds of being in the highest than lowest quartile of total current meat consumption (adjusted OR = 21.36, p = 0.001). 

 

 

Edited by Darryl, 19 January 2017 - 04:32 PM.

[normalizing]

this is recent i read about the conversion of active metabolites of ginseng done depending of your microbiota; http://pubs.acs.org/...cs.jafc.6b04848

 

i dont think humans harbor bifidobacterium animalis, but it seems to convert ginseng metabolites more active. just another interesting article of how medicinal plans can actually work depending on what bacteria you harbor

[albedo]

 

albedo same question i asked there, what is the type of bacteria to do this? the article does mention specifically this, not all bacteria does it and most people might not have that specific type. yet, we do not even know which type that is!

I did not have time yet to dig into EPFL's paper but found this study which reportedly is the first to demonstrate a pure strain producing urolithins (but for urolithin A the authors also say other bacteria might be needed)

 

"...The isolate belongs to a new species described as Gordonibacter urolithinfaciens, sp. nov. The type strain of the Gordonibacter genus, Gordonibacter pamelaeae DSM 19378(T), was also demonstrated to produce urolithins...." (bold mine)

 

Description of urolithin production capacity from ellagic acid of two human intestinal Gordonibacter species.

http://www.ncbi.nlm....pubmed/24909569

 

The Gordonibacter bacteria taxonomy description is here:

http://www.ncbi.nlm....=Info&id=657308

 

Related and relevant to this thread is that "...The potential systemic biological effects of pomegranate juice ingestion should be attributed to the colonic microflora metabolites rather than to the polyphenols present in the juice..."

http://www.ncbi.nlm....ubmed/15309440/

 

In relation to the above discussion on having or not the right strain (Gordonibacter) reading quickly the abstract of the following well conducted study (sorry I do not have access to the full text!) might suggest that, even if we have extremely little of those, consumption of pomegranate might strongly increase their population, explaining both the CVD differentiation of benefits (as in the paper) as well as the muscular health via mitophagy. As for Akkermansia, Gordonibacteria might be researched one day as a supplelemnt probiotioc. I also recollect a suggestion made also above that pomegranate is one of the ways to increase Akkermansia.

 

González-sarrías A, García-villalba R, Romo-vaquero M, et al. Clustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate: A randomised clinical trial. Mol Nutr Food Res. 2016

 

"The pomegranate lipid-lowering properties remain controversial, probably due to the interindividual variability in polyphenol (ellagitannins) metabolism.

OBJECTIVE:

We aimed at investigating whether the microbial-derived ellagitannin-metabolizing phenotypes, i.e. urolithin metabotypes A, (UM-A), B (UM-B) and 0 (UM-0), influence the effects of pomegranate extract (PE) consumption on eighteen cardiovascular risk biomarkers in healthy overweight-obese individuals.

METHODS AND RESULTS:

A double-blind, cross-over, dose-response, randomised, placebo-controlled trial was conducted. The study (POMEcardio) consisted of 2 test-phases (dose-1 and dose-2, lasting 3 weeks each) and a 3-week washout period between each phase. Forty nine participants (BMI>27 kg/m2 ) daily consumed one (dose-1, 160 mg phenolics/day) or four (dose-2, 640 mg phenolics/day) PE or placebo capsules. Notably, UM-B individuals showed the highest baseline cardiovascular risk. After dose-2, total-cholesterol (-15.5±3.7%), LDL-cholesterol (-14.9±2.1%), small-LDL-cholesterol (-47±7%), non-HDL-cholesterol (-11.3±2.5%), apolipoprotein-B (-12±2.2%) and oxidised-LDL-cholesterol (-24±2.5%) dose-dependently decreased (P<0.05) but only in UM-B subjects. These effects were partially correlated with urolithin production and the increase of Gordonibacter levels. Three (50%) non-producers (UM-0) became producers following PE consumption.

CONCLUSIONS:

Urolithin metabotype (UM) clustering suggests a personalised effect of ellagitannin-containing foods and could explain the controversial pomegranate benefits. Research on the specific role of urolithins and the microbiota associated to each UM is warranted. This article is protected by copyright. All rights reserved."(bold mine)

[normalizing]

ok i have to post this; http://www.ergo-log....e-bacteria.html as it is the very first time i have seen a bacteria from cheese (animal product) to actually benefit gut health and enhance lifespan, very interesting

[albedo]

The following study on the much studied interaction between Alzheimer's Disease and microbiome seems important: One of the authors, Frida Fåk Hållenius, says:

 

"Our study is unique as it shows a direct causal link between gut bacteria and Alzheimer’s disease. It was striking that the mice which completely lacked bacteria developed much less plaque in the brain”.“The results mean that we can now begin researching ways to prevent the disease and delay the onset. We consider this to be a major breakthrough as we used to only be able to give symptom-relieving antiretroviral drugs.”

 

Harach T, Marungruang N, Duthilleul N, et al. Reduction of Abeta amyloid pathology in APPPS1 transgenic mice in the absence of gut microbiota. Sci Rep. 2017;7:41802.

 

Gut bacteria may play a role in Alzheimer’s disease

http://www.lundunive...heimers-disease

[normalizing]

It was striking that the mice which completely lacked bacteria developed much less plaque in the brain”

 

uhm so not having bacteria seems beneficial, im confused

[Oakman]

It was striking that the mice which completely lacked bacteria developed much less plaque in the brain”

 

uhm so not having bacteria seems beneficial, im confused

 

...obviously the bacteria are clouding your judgment   

[albedo]

An updatable “evidence map” study summarizing the existing literature on dietary fiber interventions and human gut microbiota. This can be useful to research providing patterns and guideline for meta-analysis and reviews.

 

As an example, the Table 4 shows evidence that oligosaccharides, and FOS in particular, increase Bifidobacterium considered as beneficial to human health. Authors also go a step further in their sub-analysis by examining direct relationship between microbiota modulation and health outcome (e.g. lipids changes, glucose, insulin response...).

 

Sawicki CM, Livingston KA, Obin M, Roberts SB, Chung M, Mckeown NM. Dietary Fiber and the Human Gut Microbiota: Application of Evidence Mapping Methodology. Nutrients. 2017;9(2)

 

"Interest is rapidly growing around the role of the human gut microbiota in facilitating beneficial health effects associated with consumption of dietary fiber. An evidence map of current research activity in this area was created using a newly developed database of dietary fiber intervention studies in humans to identify studies with the following broad outcomes: (1) modulation of colonic microflora; and/or (2) colonic fermentation/short-chain fatty acid concentration. Study design characteristics, fiber exposures, and outcome categories were summarized. A sub-analysis described oligosaccharides and bacterial composition in greater detail. One hundred eighty-eight relevant studies were identified. The fiber categories represented by the most studies were oligosaccharides (20%), resistant starch (16%), and chemically synthesized fibers (15%). Short-chain fatty acid concentration (47%) and bacterial composition (88%) were the most frequently studied outcomes. Whole-diet interventions, measures of bacterial activity, and studies in metabolically at-risk subjects were identified as potential gaps in the evidence. This evidence map efficiently captured the variability in characteristics of expanding research on dietary fiber, gut microbiota, and physiological health benefits, and identified areas that may benefit from further research. We hope that this evidence map will provide a resource for researchers to direct new intervention studies and meta-analyses."

[albedo]

It was striking that the mice which completely lacked bacteria developed much less plaque in the brain”

 

uhm so not having bacteria seems beneficial, im confused

 

I see your point Hazy, but be aware not falling into the pitfalls of bad logic and do not be confused.

 

The logic here is to leverage the research results to see which are the possible therapeutic targets, i.e. how you translate the research into clinic and find causative links. I would guess shifting gut microbiota population might be one target, surely not eliminating it (at least as far as we remain humans !).

 

It looks to me that, by following the same flawed logic, than you could say not breathing could be an intervention target to avoid mitochondrial damage by oxidative stress which, when compensatory systems start failing due to aging, might bring to pathology and death. Would you seriously consider not breathing? We have damage building up by the very reason we live ;-)

 

[normalizing]

yeah not breathing will suspend further deterioration if you can manage to live without it heh but i can tell its better to slow down metabolism as much as possible and hibernate if possible and thats a good way to extend lifespan as many creatures who can do this live long and im pretty sure their microbiota pretty much dies out in such states

Edited by hazy, 22 February 2017 - 09:02 PM.

[normalizing]

ok this is an interesting article i found about today; http://www.nutraingr...to-centenarians

[albedo]

Thank you Hazy. Interesting despite a clear limitation is they do not address the causation of the changes. There are hints to nutrients and decreasing intestinal function but not conclusive. There are several reference to the works on centenarians and inflammaging (Franceschi et al) also discussed earlier in this thread.

 

The (open access) original paper is here:

Odamaki T, Kato K, Sugahara H, et al. Age-related changes in gut microbiota composition from newborn to centenarian: a cross-sectional study. BMC Microbiol. 2016;16:90.

 

 

[normalizing]

this new article says no benefit adding probiotics eating well already, and it might even impair your memory; http://www.medicalne...ases/316402.php

[Nate-2004]

this new article says no benefit adding probiotics eating well already, and it might even impair your memory; http://www.medicalne...ases/316402.php

 

This is disconcerting, considering that I ate yogurt and took probiotics every day for over a year and a half and it helped considerably with depression. Apparently so much so that my diet has since improved to include a lot of smoothies like this one lately. I also lost 10 lbs of fat in the past couple months or so (I have a percentage scale).

[albedo]

I liked your findings Hazy. I will try and get hold of the paper which is not open. In any case I would be cautious about pharmaceutical dosage of everything, incl. probiotics. We have a dose response in everything we ingest and tailoring is necessary. VSL#3 is very high potency prescribed in pathological conditions such as ulcerative colitis, irritable bowel syndrome and an ileal pouch: “ …VSL#3 formulations contain from 225 billion to 900 billion bacteria per serving (available by prescription)…” (1) and from what I understand from the abstract it is likely effective in those conditions implied by dysbiosis. Moreover from the abstract I understand there are distinctions on the type of memory affected (place vs. object). What about strain and strain displacement in normal conditions? What about host and microbiota genetic make up? What about replication and translation to humans? My common sense will tell me to continue (i) going for the best pre-biotics diet first, (ii) use a good probiotic when that is really welcome, e.g. before and after your antibiotic course and that is likely increasing with age and infection risks, 20-30 billion CFU might be sufficient (I personally use a 30 billion CFU Theralac once per week), (iii) test efficacy also looking at your regularity and comfort i.e. try to have regular bowel movements (I normally go for two and quite often 3 after my meals, coffee is a good initiator), (iv) look at VSL#3 in special conditions and talk to the right MD specialist first and (v) follow these research results for replication and more evidence and if i need to change I will. There are counter-examples too, such as  Misra S, Medhi B. Role of probiotics as memory enhancer. Indian J Pharmacol. 2013;45(3):311-2. just to pick one.

As usual, just IMHO ....

 

(1) https://vsl3.com/about-vsl/

[albedo]

As we are on microbiome and assuming the risk of sounding really disagreeable (!) I think it is important also to to check how your stool looks like which is a good indicator of transit time and gut health.

You might know already the Bristol Stool Chart from the original work of 1997. If not it might be good to have a look:

Lewis SJ, Heaton KW. Stool form scale as a useful guide to intestinal transit time. Scand J Gastroenterol. 1997;32(9):920-4.

E.g. see here for some general explications

 

 

[albedo]

A nice recent review:

 

Singh RK, Chang HW, Yan D, et al. Influence of diet on the gut microbiome and implications for human health. J Transl Med. 2017;15(1):73.

https://www.ncbi.nlm...pubmed/28388917

 

"Recent studies have suggested that the intestinal microbiome plays an important role in modulating risk of several chronic diseases, including inflammatory bowel disease, obesity, type 2 diabetes, cardiovascular disease, and cancer. At the same time, it is now understood that diet plays a significant role in shaping the microbiome, with experiments showing that dietary alterations can induce large, temporary microbial shifts within 24 h. Given this association, there may be significant therapeutic utility in altering microbial composition through diet. This review systematically evaluates current data regarding the effects of several common dietary components on intestinal microbiota. We show that consumption of particular types of food produces predictable shifts in existing host bacterial genera. Furthermore, the identity of these bacteria affects host immune and metabolic parameters, with broad implications for human health. Familiarity with these associations will be of tremendous use to the practitioner as well as the patient."

 

 diet bacterial genera.PNG   115.51KB   0 downloads

 

 fibers effect.PNG   166.77KB   0 downloads

 

 mediterranean.PNG   133.93KB   0 downloads

 

 

 

[to age or not to age]

I read a few articles/papers which I don't have links to which indicate that rapamycin impacts the microbiome, in ways not initially understood.

[normalizing]

rapamycin is immunosuppresant, it probably kills beneficial bacteria or muting them to not cause immune responses but ive never read about it i just speculate

[normalizing]

just by accident today, i found another one that works in similar fashion, it disrupts and slows down for a while the beneficial bacterium for a better cognitive state in the man; https://en.wikipedia...neuroprotective

 

its an antibiotic, with amazing beneficial properties

[albedo]

 

 

albedo same question i asked there, what is the type of bacteria to do this? the article does mention specifically this, not all bacteria does it and most people might not have that specific type. yet, we do not even know which type that is!

I did not have time yet to dig into EPFL's paper but found this study which reportedly is the first to demonstrate a pure strain producing urolithins (but for urolithin A the authors also say other bacteria might be needed)

 

"...The isolate belongs to a new species described as Gordonibacter urolithinfaciens, sp. nov. The type strain of the Gordonibacter genus, Gordonibacter pamelaeae DSM 19378(T), was also demonstrated to produce urolithins...." (bold mine)

 

Description of urolithin production capacity from ellagic acid of two human intestinal Gordonibacter species.

http://www.ncbi.nlm....pubmed/24909569

 

The Gordonibacter bacteria taxonomy description is here:

http://www.ncbi.nlm....=Info&id=657308

 

Related and relevant to this thread is that "...The potential systemic biological effects of pomegranate juice ingestion should be attributed to the colonic microflora metabolites rather than to the polyphenols present in the juice..."

http://www.ncbi.nlm....ubmed/15309440/

 

In relation to the above discussion on having or not the right strain (Gordonibacter) reading quickly the abstract of the following well conducted study (sorry I do not have access to the full text!) might suggest that, even if we have extremely little of those, consumption of pomegranate might strongly increase their population, explaining both the CVD differentiation of benefits (as in the paper) as well as the muscular health via mitophagy. As for Akkermansia, Gordonibacteria might be researched one day as a supplelemnt probiotioc. I also recollect a suggestion made also above that pomegranate is one of the ways to increase Akkermansia.

 

González-sarrías A, García-villalba R, Romo-vaquero M, et al. Clustering according to urolithin metabotype explains the interindividual variability in the improvement of cardiovascular risk biomarkers in overweight-obese individuals consuming pomegranate: A randomised clinical trial. Mol Nutr Food Res. 2016

 

"The pomegranate lipid-lowering properties remain controversial, probably due to the interindividual variability in polyphenol (ellagitannins) metabolism.

OBJECTIVE:

We aimed at investigating whether the microbial-derived ellagitannin-metabolizing phenotypes, i.e. urolithin metabotypes A, (UM-A), B (UM-B) and 0 (UM-0), influence the effects of pomegranate extract (PE) consumption on eighteen cardiovascular risk biomarkers in healthy overweight-obese individuals.

METHODS AND RESULTS:

A double-blind, cross-over, dose-response, randomised, placebo-controlled trial was conducted. The study (POMEcardio) consisted of 2 test-phases (dose-1 and dose-2, lasting 3 weeks each) and a 3-week washout period between each phase. Forty nine participants (BMI>27 kg/m2 ) daily consumed one (dose-1, 160 mg phenolics/day) or four (dose-2, 640 mg phenolics/day) PE or placebo capsules. Notably, UM-B individuals showed the highest baseline cardiovascular risk. After dose-2, total-cholesterol (-15.5±3.7%), LDL-cholesterol (-14.9±2.1%), small-LDL-cholesterol (-47±7%), non-HDL-cholesterol (-11.3±2.5%), apolipoprotein-B (-12±2.2%) and oxidised-LDL-cholesterol (-24±2.5%) dose-dependently decreased (P<0.05) but only in UM-B subjects. These effects were partially correlated with urolithin production and the increase of Gordonibacter levels. Three (50%) non-producers (UM-0) became producers following PE consumption.

CONCLUSIONS:

Urolithin metabotype (UM) clustering suggests a personalised effect of ellagitannin-containing foods and could explain the controversial pomegranate benefits. Research on the specific role of urolithins and the microbiota associated to each UM is warranted. This article is protected by copyright. All rights reserved."(bold mine)

 

Again on the interindividual differentiation: "...Inter-individual variation is also apparent in the conversion of dietary ellagitannins and ellagic acid to the gut microbial derivatives urolithins. Subjects can be divided into three main phenotypic groups. Group A (25–80% of subjects depending on the trial) produces only urolithin A conjugates, and group B (10–50% of subjects) produces isourolithin A and/or B as well as urolithin A, whereas group 0 (5–25% of subjects) produces no detectable urolithins [97]...."

 

Rowland I, Gibson G, Heinken A, et al. Gut microbiota functions: metabolism of nutrients and other food components. Eur J Nutr. 2017

http://link.springer...0394-017-1445-8

 

Look also at the well inclusive Tables 1 and 2 proving the % of daily reference intake of B vitamins that could be provided by the gut microbiota and the polyphenol metabolism.

 

 Gut vitamins.PNG   48.59KB   0 downloads

 Gut polyphenols.PNG   93.75KB   0 downloads

 

[Bryan_S]

Gut bacteria affect ageing

April 19, 2017

 

Are we going to all become poo eaters?

 

https://medicalxpres...ect-ageing.html

 

It is still not clear how exactly the microbes affect longevity. "It is possible that an ageing immune system is less effective at protecting the microorganisms in the intestines, with the result that there is a higher prevalence of pathogens in older guts. The gut microbiota in a young organism could help to counter this and therefore support the immune system and prevent inflammation. This could lead to longer life expectancy and better health," says Valenzano.

 

http://biorxiv.org/c...120980.full.pdf

[albedo]

 

Gut bacteria affect ageing

April 19, 2017

 

Are we going to all become poo eaters?

 

https://medicalxpres...ect-ageing.html

 

It is still not clear how exactly the microbes affect longevity. "It is possible that an ageing immune system is less effective at protecting the microorganisms in the intestines, with the result that there is a higher prevalence of pathogens in older guts. The gut microbiota in a young organism could help to counter this and therefore support the immune system and prevent inflammation. This could lead to longer life expectancy and better health," says Valenzano.

 

http://biorxiv.org/c...120980.full.pdf

 

 

Fully agree it is not yet clear but more and more results find correlations between aging and microbiome evolution during lifespan. The theorists of "inflammaging" such as Franceschini, Biagi et al. are progressing in this understanding where typically the issue is then which comes first and what is cause of what. E.g. see their nice study (and the follow-ons):

 

Rampelli S, Candela M, Turroni S, et al. Functional metagenomic profiling of intestinal microbiome in extreme ageing. Aging (Albany NY). 2013;5(12):902-12.

https://www.ncbi.nlm...pubmed/24334635

 

"Age-related alterations in human gut microbiota composition have been thoroughly described, but a detailed functional description of the intestinal bacterial coding capacity is still missing. In order to elucidate the contribution of the gut metagenome to the complex mosaic of human longevity, we applied shotgun sequencing to total fecal bacterial DNA in a selection of samples belonging to a well-characterized human ageing cohort. The age-related trajectory of the human gut microbiome was characterized by loss of genes for shortchain fatty acid production and an overall decrease in the saccharolytic potential, while proteolytic functions were more abundant than in the intestinal metagenome of younger adults. This altered functional profile was associated with a relevant enrichment in “pathobionts”, i.e. opportunistic pro-inflammatory bacteria generally present in the adult gut ecosystem in low numbers. Finally, as a signature for long life we identified 116 microbial genes that significantly correlated with ageing. Collectively, our data emphasize the relationship between intestinal bacteria and human metabolism, by detailing the modifications in the gut microbiota as a consequence of and/or promoter of the physiological changes occurring in the human host upon ageing."

 

Even supposedly anti-aging drugs such metforms might plausibly act mediating the microbiota changes. E.g. see:

 

López-otín C, Galluzzi L, Freije JM, Madeo F, Kroemer G. Metabolic Control of Longevity. Cell. 2016;166(4):802-21.

http://www.cell.com/...8674(16)30981-3

 

"... It appears therefore plausible that metformin mediates part of its antidiabetic and enigmatic anticancer effects through alterations in the microbiome, which has a central role in healthy aging..."

 

 

 

 

 

Edited by albedo, 19 April 2017 - 09:14 PM.

[Bryan_S]

albedo,

 

I just had 2 rounds of antibiotics for a tooth issue some weeks back. If I'd been on top of that purging episode I was primed to reseed my microbiome. I really hate antibiotics but there are times when you can take advantage of a bad situation and reset your flora but what probiotics can we concentrate on that will help us establish a "younger gut profile?"

[normalizing]

just by accident today, i found another one that works in similar fashion, it disrupts and slows down for a while the beneficial bacterium for a better cognitive state in the man; https://en.wikipedia...neuroprotective

 

its an antibiotic, with amazing beneficial properties

 

this still plagues me. but i was wondering this, since antibiotics can mutate bacteria in such way to become resistant to them, why is that negative for our beneficial flora? it should actually mutate and make them stronger, or whats up with that? only the bad guys can mutate and become better towards antibiotics??

[albedo]

albedo,

 

I just had 2 rounds of antibiotics for a tooth issue some weeks back. If I'd been on top of that purging episode I was primed to reseed my microbiome. I really hate antibiotics but there are times when you can take advantage of a bad situation and reset your flora but what probiotics can we concentrate on that will help us establish a "younger gut profile?"

 

The problem is I do not know what a younger gut profile actually is. I think we are far to be able to define one assuming that makes sense. My only current thinking based on some evidence is that after a stabilization of the gut flora diversity happening around 12yro there is a decline in diversity with aging.  Some peculiar shift is also happening in extremely longevity (100+) gut microbiota. There are strains already known to be beneficial and other emerging such as Gordonibacteria for mitophagy (via the Urolithin A production) and Akkermania. Diet high in fibers and resistant starches reduce “inflammaging” and favor an healthy gut. I guess the best I could do today is a Mediterranean diet possibly “potentiated” as the NuAge project is suggesting and run courses of probiotiocs from time to time when necessary. My testing is low chronic inflammation, testing for dysbiosis and a high regularity. Just my 2 cents …

 

http://www.longecity...ndpost&p=812199

http://www.cell.com/...9822(16)30338-4

http://www.longecity...ndpost&p=790852

http://www.longecity...ndpost&p=784399

Claudio Franceschi's presentation on inflammaging p. 55

http://www.longecity...ndpost&p=779160

https://www.ncbi.nlm...pubmed/25902704

 

 

 

 

 

Edited by albedo, 20 April 2017 - 05:42 PM.

[Bryan_S]

Gut bacteria give newborns infection protection, not just digestion, mouse study shows

April 20, 2017

https://medicalxpres...-digestion.html

 

I'm defiantly picking up on an overall theme here. Certain bacteria are immune protective and others are inflammatory. One might think certain strains have evolved with us and we should learn how to favor these. It's also not just our guts, we've evolved with a friendly community enveloping our skin ready to do battle with invaders as well. Within these communities the residents have evolved to protect their turf so a symbiosis exists between the host and the resident microbiome. I believe part of the problem today is we've departed from traditional vaginal birth and many protective microbes are residents of the vaginal canal and they are not being seeded upon the skin at birth. Also see the “The Old Friends Hypothesis”

 

I look to supporting evidence of such a relationship with articles like Social bees have kept their gut microbes for 80 million years

March 29, 2017 I think ours are just as well established.

 

If we want to look at the protective abilities of gut microbes we can again look to incests as a model. See Lactic acid bacterial symbionts in honeybees – an unknown key to honey’s antimicrobial and therapeutic activities In this case the protective affects of these strains of a unique group of 13 lactic acid bacteria found in fresh honey, from the honey stomach of bees. The bacteria produce a myriad of active antimicrobial compounds.

 

So I think we need to identify our unique companions and bolster those relationships. We can develop soaps and teeth cleaning products along these lines and enhance those communities that protect us.

 

There is a group focusing on figuring out who are friends are.

 

http://hmpdacc.org

"Welcome to the Data Analysis and Coordination Center (DACC) for the National Institutes of Health (NIH) Common Fund supported Human Microbiome Project (HMP). This site is the central repository for all HMP data. The aim of the HMP is to characterize microbial communities found at multiple human body sites and to look for correlations between changes in the microbiome and human health. More information can be found in the menus above and on the NIH Common Fund site."

 

As always JMHO

[normalizing]

this is one; http://www.nutraingr...nitive-function i havent heard of that type of bacteria, any information?