270 replies to this topic

[Nate-2004]

 

albedo ive never heard of this bacteria and i have never seen its consumption in any foods or drinks that humans have been consuming so im very confused as to how some people have acquired it to begin with. perhaps its natural in all of us from the get go? but then how do you even balance it and not let it die out, considering, there is absolutely no well known predominant source to re-supply it???

 

I wish I could answer to your questions! From the little I know, I think nobody has really find a way, clinically proven, to simply steer your gut microbiota to a specific profile, at least generally and in healthy populations. I also wonder if this should be attempted at all in the first place. Consider also the vast number of species in the colon (300-1000) even though 30-40 species can account for 99% of bacteria incl. colon, stomach and small intestine (here).

 

All what I am reporting here is basically research and we are far from the clinical. So while, yes, considering centenarians gut Akkermansia and others or Gordonibacter for manufacturing urolithins and also looking at what the supplementation marketing will invent with new strands, my best bet is to run a stool microbiology test first to see how you are doing and use good pre-biotics. I think a Mediterranean style diet full of vegetables and high in fibers is the best bet. Actually I would not abuse with pro-biotics to maintain an health competition between strains and good balance. Personally, I also try and keep my colon empty to avoid toxins re-absorption and try to go 3x after the 3x daily meals as an anti-cancer strategy.

 

 

I don't think that's true. Eating more yogurt and/or sauerkraut will increase the amount of bifidobacterium which is a change in profile for the positive. The degree to which my anxiety has dropped and my mood has improved over the past year and a half of making these efforts is considerable. I don't think there's anything wrong that I've noticed with changing the profile in that sense, nor would giving any akkermansia the advantage by creating more mucin. I don't know if I've succeeded in increasing akkermansia over the past 50 or so days but I've been very consistent with getting all the necessary prebiotics for it. I suppose I can find out.

[albedo]

Nate, what do you think is not true in what I wrote? I just wish to better understand your point.

[Nate-2004]

Nate, what do you think is not true in what I wrote? I just wish to better understand your point.

 

If I understood you right, you said you need some kind of competitive balance rather than giving an advantage to any particular types and therefore increasing said types. 

 

I disagree with that. I want to increase bifidobacteria as well as akkermansia, and I'd love to increase these gordoni if at all possible.

[albedo]

 

Nate, what do you think is not true in what I wrote? I just wish to better understand your point.

 

If I understood you right, you said you need some kind of competitive balance rather than giving an advantage to any particular types and therefore increasing said types. 

 

I disagree with that. I want to increase bifidobacteria as well as akkermansia, and I'd love to increase these gordoni if at all possible.

 

 

I was unclear. I stand with you with increasing bacteria as Bifidobacterium where there is plenty of evidence of benefit. I would prefer not to do it blindly and first test to check it out. I personally did it, also following symptoms of dysbiosis, and succeeded to shift results with diet and supplementation to a better profile with undetectable levels of fungi growth and no pathogens. IMHO, we are not ready clinically to define theoretically a “good profile” for health and longevity because of the vast complexity of interactions, age dependency and the existing research would need to go first to clinical in healthy humans. Diversity is key in biology and maybe even what we think being “bad” might turn to have an important role. So in this area too I strive to maintain balance with a good diet first.

 

The Importance of Microbial Diversity in Gut Health and Disease

http://articles.merc...lora.aspx#_edn4

Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school age

http://www.sciencedi...091674911008542

Diversity of the Human Intestinal Microbial Flora

http://science.scien...5728/1635.short

 

 

 

 

[albedo]

I repeat my post in the personalized nutrition thread as I believe it is also relevant here:

 

Diet–microbiota interactions as moderators of human metabolism

http://www.nature.co...ature18846.html

 

"It is widely accepted that obesity and associated metabolic diseases, including type 2 diabetes, are intimately linked to diet. However, the gut microbiota has also become a focus for research at the intersection of diet and metabolic health. Mechanisms that link the gut microbiota with obesity are coming to light through a powerful combination of translationfocused animal models and studies in humans. A body of knowledge is accumulating that points to the gut microbiota as a mediator of dietary impact on the host metabolic status. Efforts are focusing on the establishment of causal relationships in people and the prospect of therapeutic interventions such as personalized nutrition. "(bold mine)

[normalizing]

i think i posted some posts here or in another thread about antibiotics actually not being all that disruptive to the human organism and might have edge in protecting neurons and possibly exploited for alzheimers. but ill look for these again as i dont have saved links. i was confused initially about it as that would kill beneficial bacteria and it didnt make sense to me. it still doesnt, if im able to find those urls to discuss what mechanism do they exert to be so neuroprotective. also, im wondering if some natural antibiotics are also neuroprotective and looking at a profile that kills beneficial bacteria, its garlic, various tea/green, wine, berberine, curcumin etc. and they have good profile for being good for your brain BUT all of them kill beneficial bacteria, so whats the reason for this how does it work i thought killing your beneficial bacteria is bad!??

[albedo]

I was looking at interaction between gut microbiota and metformin and pop into this short review:

 

Gut Microbiota and Metabolic Disorders

http://www.ncbi.nlm....les/PMC4483604/

 

We know of the beneficial effects via the AMPK path and was wondering if benefits via the modulation of gut microbiota, which look do exist (e.g. via the increase of Akkermansia also mentioned above in this thread), are happening at much lower doses that those typically required to reduce hepatic release of glucose. A small section of the article mentions:

 

"...Metformin can also affect the intestinal microbiota of mammals. We have demonstrated that metformin is able to affect the mouse microbiota and increase the abundance of Akkermansia muciniphila, a mucin-degrading G (-) anaerobes, in the gut of experimental mice fed a HFD (Fig. 2) [34]. We also observed that the administration of A. muciniphila had similar beneficial metabolic effects to that of metformin administration: (1) increased the number of mucin-producing goblet cells was similarly found after the administration of metformin or A. muciniphila; (2) diminished regulatory T (Treg) cell numbers and elevated interleukin 1β (IL-1β) or IL-6 mRNA expression in the visceral adipose tissue of mice fed a HFD were similarly reversed after the administration of metformin or A. muciniphila. Mucin has recently been shown to enhance delivery of tolerogenic immunoregulatory signal to the intestinal epithelium by forming galectin-3-dectin-1-FcγRIIB complex besides its classical role as a physical barrier [35] This study therefore underscores that drugs, such as metformin, might exert therapeutic effects, at least in part by modulating the gut micriobiota..." (bold mine)

 

See also this, I will look if I can find a dose response:

 

An increase in the Akkermansia spp. population induced by metformin treatment improves glucose homeostasis in diet-induced obese mice.

http://www.ncbi.nlm....ubmed/23804561/

 

Btw, for the time being I am continuing with a 250 mg/day dose, I admit w/o a strong rationale. All known markers after 1.5 years look in check at this dosage.

 

 

Edited by albedo, 07 August 2016 - 11:30 AM.

[Nate-2004]

Btw, for the time being I am continuing with a 250 mg/day dose, I admit w/o a strong rationale. All known markers after 1.5 years look in check at this dosage.

 

Where are you getting metformin isn't that prescription only?

[APBT]

A clinical update on the significance of the gut microbiota in systemic autoimmunity

Attached Files

•  A clinical update on the significance of the gut microbiota in systemic autoimmunity.pdf   759.31KB   13 downloads

[albedo]

Thank you APBT for posting here this informative paper on immunity. I also wish here to refer to an old thread you started where I could re-discover good information, in particular on pro- and pre-biotics.

 

Just to add to my previous post, a more detailed review on metformin with a much larger section on metformin and the microbiota is here focusing "...on the key role of the microbiota in regulating age-associated morbidities and a potential role for metformin to modulate its function..."

[normalizing]

in short ,so metformin is one drug to boost the bacteria that can produce urolithins?

[albedo]

in short ,so metformin is one drug to boost the bacteria that can produce urolithins?

 

Maybe, but it looks to me jumping too fast to a simple conclusion and I am not sure from where you infer that.

 

It is probably a matter of balance between different strands, e.g. Gordonibacteria (afaik not yet associated to metformin though), shown to increase urolithins as indicated above (1), Lactobacilli, increased by metformin in rats on high fat diet and improving glucose uptake (2), and different paths, e.g. said glucose uptake by Akkermansia and Lactobacilli, reduced inflammation, and improved glycemic control insulin resistance (2).

 

Moreover, “…Whether changes in the structure of the microbiota result directly from high concentrations of the drug in the intestine or indirectly from metabolites resulting from the host upon metformin treatment remains to be elucidated...” (2)

 

(1) http://www.ncbi.nlm.nih.gov/pubmed/24909569

(2) http://www.ncbi.nlm.nih.gov/pubmed/26475449

 

[albedo]

Speculating a bit about the future and before we will see medical nanobots doing specific tasks in our bodies we will be able to engineer bacteria. The following gives a glimpse to what is becoming possible already today using the CRISPR genetic engineering technology:

 

"...The applications of this set of tools are enormous and break ground for a new era of engineered chassis organisms that can be used to build microbiomebased diagnostics and therapeutics..." (1)

 

(1) A Toolbox for Microbiome Engineering

http://dx.doi.org/10...els.2015.07.003

 

"...For microbiome engineering applications, the ability to precisely modulate gene expression in commensal organisms should enable functional studies of the microbiome, non-invasive monitoring of in vivo environments, and long-term targeted therapeutics..." (2)

 

(2) Programming a Human Commensal Bacterium, Bacteroides thetaiotaomicron, to Sense and Respond to Stimuli in the Murine Gut Microbiota

http://www.cell.com/...4712(15)00006-X

 

 

[albedo]

On the impact on insulin sensitivity (pay-walled):

 

Human gut microbes impact host serum metabolome and insulin sensitivity

http://www.nature.co...ature18646.html

 

Abstract."Insulin resistance is a forerunner state of ischaemic cardiovascular disease and type 2 diabetes. Here we show how the human gut microbiome impacts the serum metabolome and associates with insulin resistance in 277 non-diabetic Danish individuals. The serum metabolome of insulin-resistant individuals is characterized by increased levels of branched-chain amino acids (BCAAs), which correlate with a gut microbiome that has an enriched biosynthetic potential for BCAAs and is deprived of genes encoding bacterial inward transporters for these amino acids. Prevotella copri and Bacteroides vulgatus are identified as the main species driving the association between biosynthesis of BCAAs and insulin resistance, and in mice we demonstrate that P. copri can induce insulin resistance, aggravate glucose intolerance and augment circulating levels of BCAAs. Our findings suggest that microbial targets may have the potential to diminish insulin resistance and reduce the incidence of common metabolic and cardiovascular disorders." (bold mine)

 

[APBT]

FULL TEXT:

 

Attached Files

•  HUMAN GUT MICROBES IMPACT HOST SERUM METABOLOME AND INSULIN SENSITIVITY.pdf   1.79MB   5 downloads

[albedo]

An interesting view shared by Tim Spector on the Cell Symposium on Aging and Metabolism of July 10–12 in Spain (http://www.cell-symp...metabolism.com/). I will look for more work of Spector in this area:

 

"Over the last 20 years I have studied most of the “omics” and their role in aging, and they have a gentle correlation with increasing age from 40 to 90. These include methylation, telomere length, gene expression, proteomics, metabolomics, and glycomics. But one omic appears to be different: our gut microbiome. Our 100 trillion gut microbes have 200 times more genes than we do, each capable of producing a huge range of proteins and metabolites that regulate our metabolism and immune systems. Combined data from the American/British gut projects and our UK twins show little age effects until after the age of 75, when there is a dramatic loss of microbe species. This strongly predicts frailty and co-morbidities. I am fascinated to see if this loss of beneficial anti-inflammatory species is the consequence of the worsening diet and nutrition in old people or the possible cause of the tipping point for the faltering biological systems in many elderly folk. Either way, we can learn how to improve nutrition in the elderly, and finding the beneficial microbes that are responsible for protecting us against old age problems opens the door, eventually, for novel therapies as well the immediate option of starting trials of probiotics to extend disease-free aging."

http://www.cell.com/...4131(16)30239-X

 

The meeting brings together an amazing set of experts on Aging. Look at all the shared views.

[albedo]

Starving our Microbial Self: The Deleterious Consequences of a Diet Deficient in Microbiota-Accessible Carbohydrates

 

"The gut microbiota of a healthy person may not be equivalent to a healthy microbiota. It is possible that the Western microbiota is actually dysbiotic and predisposes individuals to a variety of diseases. The asymmetric plasticity between the relatively stable human genome and the more malleable gut microbiome suggests that incompatibilities between the two could rapidly arise. The Western lifestyle, which includes a diet low in microbiota-accessible carbohydrates (MACs), has selected for a microbiota with altered membership and functionality compared to those of groups living traditional lifestyles. Interactions between resident microbes and host leading to immune dysregulation may explain several diseases that share inflammation as a common basis. The low-MAC Western diet results in poor production of gut microbiota-generated short-chain fatty acids (SCFAs), which attenuate inflammation through a variety of mechanisms in mouse models. Studies focused on modern and traditional societies, combined with animal models, are needed to characterize the connection between diet, microbiota composition, and function. Differentiating between an optimal microbiota, one that increases disease risk, and one that is causative or potentiates disease will be required to further understand both the etiology and possible treatments for health problems related to microbiota dysbiosis."

[normalizing]

https://www.scienced...60831142914.htm

[albedo]

Gut Microbiota: A Contributing Factor to Obesity

https://www.ncbi.nlm...les/PMC5003832/

 

"Obesity, a global epidemic of the modern era, is a risk factor for cardiovascular diseases (CVD) and diabetes. The pervasiveness of obesity and overweight in both developed as well as developing populations is on the rise and placing a huge burden on health and economic resources. Consequently, research to control this emerging epidemic is of utmost importance. Recently, host interactions with their resident gut microbiota (GM) have been reported to be involved in the pathogenesis of many metabolic diseases, including obesity, diabetes, and CVD. Around 10(14) microorganisms reside within the lower human intestine and many of these 10(14) microorganisms have developed mutualistic or commensal associations with the host and actively involved in many physiological processes of the host. However, dysbiosis (altered gut microbial composition) with other predisposing genetic and environmental factors, may contribute to host metabolic disorders resulting in many ailments. Therefore, delineating the role of GM as a contributing factor to obesity is the main objective of this review. Obesity research, as a field is expanding rapidly due to major advances in nutrigenomics, metabolomics, RNA silencing, epigenetics, and other disciplines that may result in the emergence of new technologies and methods to better interpret causal relationships between microbiota and obesity."

[Brock]

interesting hypothesis. Taking a look at the firmicutes stain it has the ability to make greater use of caloric energy. That being said it is commonly thought to be the dividing factor for those struggling to lose weight after becoming obese.This shift in microbiota is outlined by dr. perlmutter in his book Brainmaker. One could then draw a link from greater energy consumption to increased free radicals, leading to greater mortality. Where adaptation normally kicks in to prevent oxidative stress the obese individuals are dealing with downed defences preventing full recovery to adapt and overcome. I put together a grouped process of colon cleansing foods which delves into the bacteroidetes strain. It is a constant battle between the 2 colonizing strains in your gut bacteroidetes v.s firmicutes.  

[APBT]

Heritable components of the human fecal microbiome are associated with visceral fat

 

FULL TEXT:  http://genomebiology...3059-016-1052-7

 

Abstract

Background

Variation in the human fecal microbiota has previously been associated with body mass index (BMI). Although obesity is a global health burden, the accumulation of abdominal visceral fat is the specific cardio-metabolic disease risk factor. Here, we explore links between the fecal microbiota and abdominal adiposity using body composition as measured by dual-energy X-ray absorptiometry in a large sample of twins from the TwinsUK cohort, comparing fecal 16S rRNA diversity profiles with six adiposity measures.

 

Results

We profile six adiposity measures in 3666 twins and estimate their heritability, finding novel evidence for strong genetic effects underlying visceral fat and android/gynoid ratio. We confirm the association of lower diversity of the fecal microbiome with obesity and adiposity measures, and then compare the association between fecal microbial composition and the adiposity phenotypes in a discovery subsample of twins. We identify associations between the relative abundances of fecal microbial operational taxonomic units (OTUs) and abdominal adiposity measures. Most of these results involve visceral fat associations, with the strongest associations between visceral fat and Oscillospira members. Using BMI as a surrogate phenotype, we pursue replication in independent samples from three population-based cohorts including American Gut, Flemish Gut Flora Project and the extended TwinsUK cohort. Meta-analyses across the replication samples indicate that 8 OTUs replicate at a stringent threshold across all cohorts, while 49 OTUs achieve nominal significance in at least one replication sample. Heritability analysis of the adiposity-associated microbial OTUs prompted us to assess host genetic-microbe interactions at obesity-associated human candidate loci. We observe significant associations of adiposity-OTU abundances with host genetic variants in the FHIT, TDRG1 and ELAVL4 genes, suggesting a potential role for host genes to mediate the link between the fecal microbiome and obesity.

 

Conclusions

Our results provide novel insights into the role of the fecal microbiota in cardio-metabolic disease with clear potential for prevention and novel therapies.

 

[APBT]

STEM-Talk PODCAST: Dr. Alessio Fasano discusses the gut microbiome and how it affects our health

https://www.ihmc.us/...alk/episode-20/

 

[Nate-2004]

STEM-Talk PODCAST: Dr. Alessio Fasano discusses the gut microbiome and how it affects our health

https://www.ihmc.us/...alk/episode-20/

Brilliantly informative. It sucks that we know so little yet know so much so far but he's probably right, in two years time we will likely know twice as much about this aspect of our biology.

I'm not doing too much about gut health but what I am doing is taking glutamine, n-acetyl-glucosamine, ellagic acid and probiotics. He talks about oggliosaccharides and how they feed the good bacteria in infants from breast milk but recently I stopped taking the FOS until we know more because I heard that can feed the bad as much as the good. So just the mucin producing and uroliithin A producing stuff for now I guess.

[Darryl]

I suspect systemic exposure to endotoxins originating from the gut is the inflammation initiator we have most control over, and many dietary approaches that reduce inflammation and chronic disease (low fat, sugar, and alcohol, high whole grain, legume, fruit and vegetable consumption) may have their primary effects through modulating the microbiota and reducing intestinal permeability to endotoxin. Looking just at the reports on aging:

 

Ghosh et al, 2015. Elevated muscle TLR4 expression and metabolic endotoxemia in human aging. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 70(2), pp.232-246.

 

We examined whether older, healthy (lean, community-dwelling) participants have altered signaling flux through toll-like receptor 4 (TLR4), a key mediator of innate and adaptive immune responses. We also examined whether a 4-month aerobic exercise program would have an anti-inflammatory effect by reducing TLR4 expression and signaling. At baseline, muscle TLR4, nuclear factor κB p50 and nuclear factor κB p65 protein content, and c-Jun N-terminal kinase phosphorylation were significantly elevated in older versus young participants. The plasma concentration of the TLR4 agonist lipopolysaccharide and its binding protein also were significantly elevated in older participants, indicative of metabolic endotoxemia, which is a recently described phenomenon of increased plasma endotoxin level in metabolic disease. These alterations in older participants were accompanied by decreased insulin sensitivity, quadriceps muscle volume, and muscle strength. The exercise training program increased insulin sensitivity, without affecting quadriceps muscle volume or strength. Muscle TLR4, nuclear factor κB, and c-Jun N-terminal kinase, and plasma lipopolysaccharide and lipopolysaccharide binding protein were not changed by exercise.

 

Kim, 2016. Gut microbiota lipopolysaccharide accelerates inflamm-aging in mice. BMC microbiology,16(1), p.1.

 

Levels of plasmatic and fecal lipopolysaccharides were higher in aged mice. Aging induced the expression of p16 and the activation of nuclear factor-kappa B (NF-κB) in the colon of aged mice. Interestingly, the expression level of sterile α-motif domain- and HD domain-containing protein 1 (SAMHD1) in the colon was higher in aged mice than in young mice, while cyclin-dependent kinase-2 and cyclin E levels were lower in aged mice than in young mice. The lipopolysaccharide fraction of fecal lysates (LFL) from young or aged mice increased p16 and SAMHD1 expression and NF-κB activation in peritoneal macrophages from wild-type mice, in a TLR4-dependent manner. However, LFLs did not induce NF-κB activation and SAMHD1 expression in peritoneal macrophages from TLR4-deficent mice, whereas they significantly induced p16 expression. Nevertheless, p16 expression was induced more potently in macrophages from WT mice than in macrophages from TLR4-deficient mice.

 

Mitchell et al, 2016. Reduced intestinal motility, mucosal barrier function, and inflammation in aged monkeys. The journal of nutrition, health & aging, pp.1-8.

Old monkeys have greater systemic inflammation and poor intestinal barrier function as compared to young monkeys

 

 

Edited by Darryl, 30 September 2016 - 10:50 PM.

[Darryl]

Cont'd

 

As for dietary interventions that increase Akkermansia and likely hence reduce intestinal permeability to endotoxins, there's plenty, and unless you've been wearing keto-diet blinders, you probably practice them as healthy diet goals. Effect sizes for prebiotic oligosaccharides are much larger than seen with metformin.

 

Van den Abbeele et al, 2011. Arabinoxylans and inulin differentially modulate the mucosal and luminal gut microbiota and mucin‐degradation in humanized rats. Environmental microbiology, 13(10), pp.2667-2680.

These mucins were degraded along the colon, resulting in high faecal abundances of Akkermansia muciniphila for long-chain arabinoxylan and especially inulin-treated rats.

 

FYI: arabinoxylan comprises 21% of wheat bran, 7% of whole wheat, and 2% of refined wheat flour. Wheat also has some oligofructose, though other common sources like garlic and onions have more.

 

Everard et al, 2013. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. PNAS, 110(22), pp.9066-9071.

We recently discovered that the administration of prebiotics (oligofructose) to genetically obese mice increased the abundance of A. muciniphila by ∼100-fold

 

Sybille et al, 2013. The intestinal microbiota in aged mice is modulated by dietary resistant starch and correlated with improvements in host responses. FEMS microbiology ecology, 83(2), pp.299-309.

16S rRNA gene amplicon sequencing was applied to determine the structure of the bacterial communities in the ceca of 20-month-old healthy mice fed energy-controlled diets containing 0, 18, or 36% type 2 resistant starch (RS) from high-amylose maize (HAM-RS2). The cecal microbiota of mice fed a diet depleted in RS and containing the readily digestible carbohydrate amylopectin were dominated by bacteria in the Firmicutes phylum and contained low levels of Bacteroidetes and Actinobacteria. In contrast, mice fed diets containing HAM-RS2 were colonized by higher levels of Bacteroidetes and Bifidobacterium, Akkermansia, and Allobaculum species in proportions that were dependent on the concentration of the dietary fiber.

 

Anhê et al. 2015. A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice. Gut, 64(6), 872-883.

Beneficial effects of cranberry extract treatment on metabolic phenotypes were associated with a robust modulation in the relative abundance of Akkermansia spp., as suggested by the higher representation (30%) of reads assigned to this genus in cranberry extract treatment metagenome at week 9 in comparison with week 1.

 

I ran out of permitted quote boxes:

Monk et al, 2016. Navy bean supplementation in obesity increases Akkermansia muciniphila abundance and attenuates obesity related impairments in gut barrier function. The FASEB Journal, 30(1 Supplement), pp.421-2.

Fecal abundance of Akkermansia muciniphila, whose abundance is inversely related to the severity of the obese phenotype, was increased in the high fat + bean diet group versus high fat diet by 20-fold.

 

Anything that increases colonic short-chain fatty acid production will increase production of the mucin that Akkermansia feeds upon, so we may be seeing indirect effects.

 

Willemsen et al, 2003. Short chain fatty acids stimulate epithelial mucin 2 expression through differential effects on prostaglandin E1 and E2 production by intestinal myofibroblasts. Gut, 52(10), pp.1442-1447.

SCFA supported a mucoprotective PG profile, reflected by an increased PGE1/PGE2 ratio in myofibroblast supernatants and increased MUC-2 expression in mono- and cocultures. Incubation with indomethacin revealed the latter to be mediated by PG.

 

Burger-van Paassen et al, 2009. The regulation of intestinal mucin MUC2 expression by short-chain fatty acids: implications for epithelial protection. Biochemical Journal, 420(2), pp.211-219.

Butyrate (at 1 mM), as well as propionate, induced an increase in MUC2 mRNA levels. MUC2 mRNA levels returned to basal levels after incubation with 5–15 mM butyrate. Interestingly, this decrease was not due to loss of RNA stability. In contrast, at concentrations of 5–15 mM propionate, MUC2 mRNA levels remained increased.

 

[APBT]

FULL TEXT:  http://www.sciencedi...304394016300775

 

 

 

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Highlights

    Interest in how diet influences brain function via the gut microbiome is growing.

Butyrate can protect the brain and enhance plasticity in neurological disease models.

Gut microbiota produce butyrate by fermenting carbohydrates in a high fiber diet.

Hypothesis: A high fiber diet can elevate butyrate to prevent/treat brain disorders.

 

Abstract

As interest in the gut microbiome has grown in recent years, attention has turned to the impact of our diet on our brain. The benefits of a high fiber diet in the colon have been well documented in epidemiological studies, but its potential impact on the brain has largely been understudied. Here, we will review evidence that butyrate, a short-chain fatty acid (SCFA) produced by bacterial fermentation of fiber in the colon, can improve brain health. Butyrate has been extensively studied as a histone deacetylase (HDAC) inhibitor but also functions as a ligand for a subset of G protein-coupled receptors and as an energy metabolite. These diverse modes of action make it well suited for solving the wide array of imbalances frequently encountered in neurological disorders. In this review, we will integrate evidence from the disparate fields of gastroenterology and neuroscience to hypothesize that the metabolism of a high fiber diet in the gut can alter gene expression in the brain to prevent neurodegeneration and promote regeneration.

 

 

 

 

[albedo]

An additional study (2015) on Akkermansia muciniphila. While not conclusive on diet -  A. Muciniphila interaction (but look also at Darryl's posts for sources) the association with healthier metabolism in humans looks confirmed:

 

 

What are the new findings?
▸Higher A. muciniphila abundance is associated with a healthier metabolic status in overweight/obese humans.
▸ There is an interaction between gut microbiomerichness, certain metagenomic species and A. muciniphila, whereby higher abundance of this species together with greater microbial gene richness are associated with a healthier metabolic status.
▸ Higher abundance of A. muciniphila at baseline is associated with greater improvement in glucose homoeostasis, blood lipids and body composition after calorie restriction.

 

Dao MC, Everard A, Aron-Wisnewsky J, et al. Akkermansia muciniphilaand improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology. Gut 2015;65:426–36. doi:10.1136/gutjnl-2014-308778

 

 

 

[Darryl]

A new study (which I don't have full access to) appears to tie together studies on protein restriction, longevity and healthy gut microbes like mucin consuming Akkermansia:

 

Holmes et al, 2016. Diet-microbiome interactions in health are controlled by intestinal nitrogen source constraints. Cell metabolism, http://dx.doi.org/10...met.2016.10.021

Highlights

• Gut microbes show a dichotomy in ecological strategy for access to nitrogen

• Beneficial microbes are overrepresented in the endogenous N source guild

• Diets that reduce availability of dietary N to microbes promote healthy aging

• Diet impact on host-microbiome interaction can be simplified for modeling

 

Summary

Diet influences health and patterns of disease in populations. How different diets do this and why outcomes of diets vary between individuals are complex and involve interaction with the gut microbiome. A major challenge for predicting health outcomes of the host-microbiome dynamic is reconciling the effects of different aspects of diet (food composition or intake rate) on the system. Here we show that microbial community assembly is fundamentally shaped by a dichotomy in bacterial strategies to access nitrogen in the gut environment. Consequently, the pattern of dietary protein intake constrains the host-microbiome dynamic in ways that are common to a very broad range of diet manipulation strategies. These insights offer a mechanism for the impact of high protein intake on metabolic health and form the basis for a general theory of the impact of different diet strategies on host-microbiome outcomes.

 

 

 

This is the same group responible for:

 

Solon-Biet et al, 2014. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Cell metabolism, 19(3), pp.418-430.

[albedo]

Cattaneo A, Cattane N, Galluzzi S, et al. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly. Neurobiol Aging. 2016;49:60-68.

 

"...Our data indicate that an increase in the abundance of a pro-inflammatory GMB taxon, Escherichia/Shigella, and a reduction in the abundance of an anti-inflammatory taxon, E. rectale, are possibly associated with a peripheral inflammatory state in patients with cognitive impairment and brain amyloidosis. A possible causal relation between GMB-related inflammation and amyloidosis deserves further investigation..."

[albedo]

 

FULL TEXT:  http://www.sciencedi...304394016300775

 

 

 

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Highlights

Interest in how diet influences brain function via the gut microbiome is growing.

Butyrate can protect the brain and enhance plasticity in neurological disease models.

Gut microbiota produce butyrate by fermenting carbohydrates in a high fiber diet.

Hypothesis: A high fiber diet can elevate butyrate to prevent/treat brain disorders.

......

 

 

While evidence is growing daily on the link between gut microbiome status and metabolic disorders as in many of the previous posts, I am also researching on the brain health (and epilepsy specifically if you happen to have interesting pointers, thank you in advance). The association study between pro- and anti-inflammatory gut microbiota and inflammation global markers, in relationship to amyloidosis and alzheimer, is also steering more research.

 

On the same line, the following study is quite impressive on autism. Obviously we have the inherent limitations of work on mouse models but if this replicates and confirms in humans, it is really major also because, being ASD a "spectrum" of disorders, the impact might be even larger than foreseen.

 

Buffington et al. Microbial reconstitution reverses maternal diet-induced social and synaptic deficits in offspring. Cell, 2016 DOI: 10.1016/j.cell.2016.06.001

 

Highlights

• Maternal high-fat diet (MHFD) induces behavioral alterations in offspring
• MHFD causes alterations in gut microbial ecology in offspring
• MHFD offspring show deficient synaptic plasticity in the VTA and oxytocin production
• L. reuteri treatment restores oxytocin levels, VTA plasticity and social behaviors