Gut Bacteria Overgrowth, Regardless Of Type, Causes Obesity

[haidut]

post 107549 I gained like 30lbs in the past two years I think from not-properly-dissolved gelatin feeding bacteria and initializing the cascade of inflammation leading to obesity.

Haidut, how can one reverse abdominal fat by dealing with bacteria? Carrots alone can't do the trick.

It really depends on what's causing the belly fat. Have you tested for cortisol? Cascara (actually emodin) is both an endotoxin and cortisol synthesis inhibitor, and it was used in animal studies to reverse obesity. Naringenin also seems to inhibit cortisol synthesis, so citrus fruit should help.
http://www.ncbi.nlm.nih.gov/pubmed/22673833
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2962821/
http://www.ncbi.nlm.nih.gov/pubmed/10072942

 

[frankfranks]

You guys continue to go on about the carrot like it's gospel. I'm pretty sure the whole carrot thing is debunked:

http://peatarianreviews.blogspot.com/20 ... eptic.html

To the extent carrot helps it's probably just a matter of the fiber improving motility in the context of an otherwise low fiber diet. It's by keeping the bacteria regularly pumped out of the tailpipe that you can reduce endotoxin.

As discussed in the link, wheat bran is probably more useful. Personally, I eat a bowl of shredded wheat for breakfast every day. It definitely helps keeps stools neat and regular, which I'm pretty sure is the best you can shoot for, without doing something weird like massive courses of antibiotics and polyethylene glycol and living in a bubble.

 

[onioneyedox]

It would be interesting to see stool analysis (such as Ubiome ) one of the "healthy peatarians" and compare it to what the paleo/ancestral people consider healthy (like here http://thegutinstitute.com/ubiome-tree ).

 

[lexis]

http://suppversity.blogspot.com/2015/11 ... iotic.html

Many Probiotics Contain Antibiotic Resistant Bacteria. Plus: Number of Live Bacteria is up to 95% Below Label Claims

 

[narouz]

Also, if you know of a beneficial mechanism through which gut bacteria acts please send me some references. I have been struggling to find evidence disproving Peat's ideas on gut bacteria and so far I am empty-handed. Combined with the study on essentiality of gut bacteria for serotonin production the case against gut bacteria is looking rather strong right now

...

Whatever toxins gets absorbed by the colon go back to the liver through the portal vein and if liver is working well it excretes these toxins. However, chronic overproduction of endotoxin and other crap we eat and gets undigested to the colon can slowly damage the liver over time. A person can even get acute hepatic failure from too much endotoxin.

Check this one out, haidut.
I've been experimenting with some different strains (probiotics).
My main problem has been palpitations--seemingly connected to when I try to appropriately dose my thyroid meds.
One (or a combo) of these stops the palpitations:
s. boulardii, l. rhamnosus, b. coagulans, and/or l. reuteri

My hypothesis is that something is going on in my gut,
causing endotoxin,
overloading the liver,
causing palpitations.

"The structural position of the liver as a bridge between the returning blood from the digestive system and the lower part of the body to the heart makes the liver an important organ for the health of the heart. A weakened and swollen or congested liver can obstruct the venous blood flow to the heart causing heart palpitations or even heart attacks. In other words a healthy liver is essential for maintaining an adequate amount of blood flow to the heart and the heart can only pump the blood it receives."
http://www1.mans.edu.eg/facphar/arabic/Newsletters/liverDisease.htm

Saccharomyces boulardii administration changes gut microbiota and reduces hepatic steatosis, low-grade inflammation, and fat mass in obese and type 2 diabetic db/db mice
http://www.ncbi.nlm.nih.gov/pubmed/24917595

Everard A1, Matamoros S1, Geurts L1, Delzenne NM1, Cani PD2.
Author information
1Université catholique de Louvain, Louvain Drug Research Institute, WELBIO (Walloon Excellence in Life Sciences and Biotechnology), Metabolism and Nutrition Research Group, Brussels, Belgium.
2Université catholique de Louvain, Louvain Drug Research Institute, WELBIO (Walloon Excellence in Life Sciences and Biotechnology), Metabolism and Nutrition Research Group, Brussels, Belgium [email protected].
Abstract
Growing evidence shows that gut microbes are key factors involved in the regulation of energy homeostasis, metabolic inflammation, lipid metabolism, and glucose metabolism. Therefore, gut microbiota modulations caused by selectively fermented oligosaccharides or probiotic bacteria constitute an interesting target in the physiopathology of obesity. However, to date, no probiotic yeast has been investigated in this context. Therefore, our study aimed to evaluate the impact of the most-studied probiotic yeast (i.e., Saccharomyces boulardii Biocodex) on obesity and associated metabolic features, such as fat mass development, hepatic steatosis, and low-grade inflammation, in obese mice. S. boulardii was administered daily by oral gavage to leptin-resistant obese and type 2 diabetic mice (db/db) for 4 weeks. We found that S. boulardii-treated mice exhibited reduced body weight, fat mass, hepatic steatosis, and inflammatory tone. Interestingly, these effects of S. boulardii on host metabolism were associated with local effects in the intestine. S. boulardii increased cecum weight and cecum tissue weight but also induced dramatic changes in the gut microbial composition at the phylum, family, and genus levels. These gut microbiota changes in response to S. boulardii may also be correlated with the host metabolism response. In conclusion, this study demonstrates for the first time that S. boulardii may act as a beneficial probiotic treatment in the context of obesity and type 2 diabetes.
IMPORTANCE:
To date, no probiotic yeast have been investigated in the context of obesity and type 2 diabetes. Here we found that type 2 diabetic and obese mice (db/db) treated with Saccharomyces boulardii exhibited reduced body weight, fat mass, hepatic steatosis, and inflammatory tone. These effects on host metabolism were associated with local effects in the intestine. Importantly, by using pyrosequencing, we found that S. boulardii treatment induces changes of the gut microbiota composition at the phylum, family, and genus levels. Moreover, we found that gut microbiota changes in response to S. boulardii were correlated with several host metabolism responses.
Copyright © 2014 Everard et al.
PMID: 24917595 [PubMed - indexed for MEDLINE] PMCID: PMC4056549 Free PMC Article


edit: another...

http://www.ncbi.nlm.nih.gov/pubmed/25227279

Oral administration of Saccharomyces boulardii ameliorates carbon tetrachloride-induced liver fibrosis in rats via reducing intestinal permeability and modulating gut microbial composition.
Li M1, Zhu L, Xie A, Yuan J.
Author information
Abstract
To investigate the effects of orally administrated Saccharomyces boulardii (S. boulardii) on the progress of carbon tetrachloride (CCl4)-induced liver fibrosis, 34 male Wistar rats were randomly divided into four experimental groups including the control group (n = 8), the cirrhotic group (n = 10), the preventive group (n = 8), and the treatment group (n = 8). Results showed that the liver expression levels of collagen, type I, alpha 1 (Col1A1), alpha smooth muscle actin (αSMA), transforming growth factor beta (TGF-β) and the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) increased significantly in cirrhotic rats compared with control and decreased by S. boulardii administration. Treatment of S. boulardii also attenuated the increased endotoxin levels and pro-inflammatory cytokines in CCl4-treated rats. And, these were associated with the changes of intestinal permeability and fecal microbial composition. Our study suggested that oral administration of S. boulardii can promote the liver function of CCl4-treated rats, and the preventive treatment of this probiotic yeast may decelerate the progress of liver fibrosis.

 

[messtafarian]

Peat writes according to specific conditions though so you can't take these things entirely out of context. Having a sterile gut is not really practical or realistic in the first place. So I think what he's arguing for is the idea of cleaning out gut bacteria as a therapy and not having a sterile gut all the time. The carrot salad, the coconut oil will not wipe out all bacteria but day to day the idea is to keep it under control.

 

[narouz]

post 109024 Peat writes according to specific conditions though so you can't take these things entirely out of context. Having a sterile gut is not really practical or realistic in the first place. So I think what he's arguing for is the idea of cleaning out gut bacteria as a therapy and not having a sterile gut all the time. The carrot salad, the coconut oil will not wipe out all bacteria but day to day the idea is to keep it under control.

Well...for instance (an instance where I've found, what seems to me, a blank spot in PeatDom):
let's say you do some tetracyclines--as many Peatians, like myself, do.
Or let's say you have a dental abscess and take a week or two course of antibiotics.
You might wonder--because of what, I guess, could be called mainstream medical thinking:
shouldn't I take some probiotics to fill the vacuum left by the antibiotics?
But then, as a Peatian, you say: hell no! any probiotics will just increase lactic acid and cause serotonin!
And so...you probably don't take the probiotics.

In my case...I don't think that Peatian strategy worked out so well
This may have something to do with the fact I don't have an appendix.

 

[messtafarian]

post 109040

post 109024

Well...for instance (an instance where I've found, what seems to me, a blank spot in PeatDom):
let's say you do some tetracyclines--as many Peatians, like myself, do.
Or let's say you have a dental abscess and take a week or two course of antibiotics.
You might wonder--because of what, I guess, could be called mainstream medical thinking:
shouldn't I take some probiotics to fill the vacuum left by the antibiotics?
But then, as a Peatian, you say: hell no! any probiotics will just increase lactic acid and cause serotonin!
And so...you probably don't take the probiotics.
This may have something to do with the fact I don't have an appendix.

In my case...I don't think that Peatian strategy worked out so well.

I am in exactly that situation at the moment. I was just on a heavy course of IV antibiotics and hesitate to take probiotics.

But for me there's another angle -- I used to work for someone somewhat famous in academic circles dealing with the gut microbiome. One of the things they were finding was that a lot of the probiotic products on the shelves did not contain anything even nearing what they said they did on their labels. That's the first problem -- how do you know you're even taking what you intend to take? There was a large mainstream american manufacturer that was buying its supplies from china and -- here is the problem-- that company was putting this stuff into capsules and on shelves without testing to make sure the bacteria were in there. Finally when these things were independently tested there were bacteria in there but not the bacteria this manufacturer was claiming it was. Point is -- the producers of these off-the-shelf probiotics are not technically sophisticated enough yet to even be sure they're selling you the right thing.

The other problem is that there probably is a kind of co-evolutionary harmony between gut flora and Us. But I promise you no one knows what that balanced gut flora exactly contains or whether there will *ever* be a way to manipulate it to induce controlled effects. In the meantime, certain bacteria in certain amounts can be extremely dangerous or lethal.

I don't think there is a hole in what peat is saying. I read him to say that it's better to have a sterile gut and allow bacteria to repopulate naturally -- and possibly very slowly using carrots and coconut oil or other mildly antimicrobial substances -- then it is to swallow a bunch of bacteria we truly know nearly nothing about.

 

[narouz]

I don't think there is a hole in what peat is saying. I read him to say that it's better to have a sterile gut and allow bacteria to repopulate naturally -- and possibly very slowly using carrots and coconut oil or other mildly antimicrobial substances -- then it is to swallow a bunch of bacteria we truly know nearly nothing about.

Yes. I suppose I should put it this way:
from a Peatian perspective, there is no hole (or blank, or gap).

To me, though...it seems like there may be.
You can go back about 2 or 3 years here on the forum
and find when Charlie did a minocycline log
and, about the same time, I tried some Peat-style antibiotics.
We both came out, shortly thereafter, with coated tongues.
We tried the Peatian answer to this--flowers of sulphur.
Didn't help me.
I can't recall with Charlie.

That coated tongue has never left me
except for brief spells while I again tried Peatian antibiotics
or other antibiotics (amoxicillin for a dental thing).
But came right back after I stopped the antibiotics.

The cleanest pink my tongue has been these last couple years or so
has been while I've been experimenting with those various probiotic strains I noted upthread
and with different prebiotics like FOS and inulin and other soluble fibers.

I really don't want to claim I know what's going on.
Just feeling my way along in the dark, sortuv, trial and error,
stepping outside the Peatian lines a bit, experimenting--
because for me I just wasn't doing well on Straight Peat.

 

[messtafarian]

So that makes sense. The other way to repopulate the gut is with starch, and I'm pretty sure that's how people were recovering from strong antibiotics before anyone had ever heard of probiotics. Quite a few people with IBS swear by "medicinal" prebiotic fibers like acacia gum. I think one explanation for IBS is that somehow either due to infection or some other kind of gut damage, there may be certain strains of gut bacteria that simply can not take hold anymore in the gut; or in the case of "antibiotic dysbiosis", one has a certain predisposition to host certain strains of bacteria over other ones.

That's where the researchers were going when I left. They believed that the gut microbiota was a phenomenon of co-evolution and were close to proving that different genetic haplotypes naturally harbored different types of bacteria. The core microbiome was usually always still there, but some strains more than others; some appeared in some genetic types and some not at all.

I don't think there is one answer with this, and I think your experiments with certain bacterial strains are really interesting. What you've done so far is much more targeted than just buying something from the drugstore, swallowing it and hoping for the best.

 

[narouz]

I thought I'd post this here
not because I'm making an argument for or against,
but just because I came across it and had never heard about it before.
I got curious about it because,
in perusing products probiotic/prebiotic
at the vitamin store
I came across this product called "FloraPhage."

Bacteriophage

A bacteriophage /ˈbækˈtɪər.i.oʊˌfeɪdʒ/ (informally, phage /ˈfeɪdʒ/) is a virus that infects and replicates within a bacterium. The term is derived from "bacteria" and the Greek: φαγεῖν (phagein), "to devour". Bacteriophages are composed of proteins that encapsulate a DNA or RNA genome, and may have relatively simple or elaborate structures. Their genomes may encode as few as four genes, and as many as hundreds of genes. Phages replicate within the bacterium following the injection of their genome into its cytoplasm. Bacteriophages are among the most common and diverse entities in the biosphere.[1]

Phages are widely distributed in locations populated by bacterial hosts, such as soil or the intestines of animals. One of the densest natural sources for phages and other viruses is sea water, where up to 9×108 virions per milliliter have been found in microbial mats at the surface,[2] and up to 70% of marine bacteria may be infected by phages.[3] They have been used for over 90 years as an alternative to antibiotics in the former Soviet Union and Central Europe, as well as in France.[4] They are seen as a possible therapy against multi-drug-resistant strains of many bacteria (see phage therapy).[5] Nevertheless, phages of Inoviridae have been shown to complicate biofilms involved in pneumonia and cystic fibrosis, shelter the bacteria from drugs meant to eradicate disease and promoting persistent infection.[6]


Classification
Bacteriophages occur abundantly in the biosphere, with different virions, genomes and lifestyles. Phages are classified by the International Committee on Taxonomy of Viruses (ICTV) according to morphology and nucleic acid.

Nineteen families are currently recognized by the ICTV that infect bacteria and archaea. Of these, only two families have RNA genomes and only five families are enveloped. Of the viral families with DNA genomes, only two have single-stranded genomes. Eight of the viral families with DNA genomes have circular genomes, while nine have linear genomes. Nine families infect bacteria only, nine infect archaea only, and one (Tectiviridae) infects both bacteria and archaea.

ICTV classification of prokaryotic (bacterial and archaeal) viruses[1]
Order Family Morphology Nucleic acid Examples
Caudovirales Myoviridae Nonenveloped, contractile tail Linear dsDNA T4 phage, Mu, PBSX, P1Puna-like, P2, I3, Bcep 1, Bcep 43, Bcep 78
Siphoviridae Nonenveloped, noncontractile tail (long) Linear dsDNA λ phage, T5 phage, phi, C2, L5, HK97, N15
Podoviridae Nonenveloped, noncontractile tail (short) Linear dsDNA T7 phage, T3 phage, P22, P37
Ligamenvirales Lipothrixviridae Enveloped, rod-shaped Linear dsDNA Acidianus filamentous virus 1
Rudiviridae Nonenveloped, rod-shaped Linear dsDNA Sulfolobus islandicus rod-shaped virus 1
Unassigned Ampullaviridae Enveloped, bottle-shaped Linear dsDNA
Bicaudaviridae Nonenveloped, lemon-shaped Circular dsDNA
Clavaviridae Nonenveloped, rod-shaped Circular dsDNA
Corticoviridae Nonenveloped, isometric Circular dsDNA
Cystoviridae Enveloped, spherical Segmented dsRNA
Fuselloviridae Nonenveloped, lemon-shaped Circular dsDNA
Globuloviridae Enveloped, isometric Linear dsDNA
Guttaviridae Nonenveloped, ovoid Circular dsDNA
Inoviridae Nonenveloped, filamentous Circular ssDNA M13
Leviviridae Nonenveloped, isometric Linear ssRNA MS2, Qβ
Microviridae Nonenveloped, isometric Circular ssDNA ΦX174
Plasmaviridae Enveloped, pleomorphic Circular dsDNA
Tectiviridae Nonenveloped, isometric Linear dsDNA

History
Since ancient times, reports of river waters having the ability to cure infectious diseases, such as leprosy, have been documented. In 1896, Ernest Hanbury Hankin reported that something in the waters of the Ganges and Yamuna rivers in India had marked antibacterial action against cholera and could pass through a very fine porcelain filter. In 1915, British bacteriologist Frederick Twort, superintendent of the Brown Institution of London, discovered a small agent that infected and killed bacteria. He believed the agent must be one of the following:

a stage in the life cycle of the bacteria;
an enzyme produced by the bacteria themselves; or
a virus that grew on and destroyed the bacteria.
Twort's work was interrupted by the onset of World War I and shortage of funding. Independently, French-Canadian microbiologist Félix d'Hérelle, working at the Pasteur Institute in Paris, announced on 3 September 1917, that he had discovered "an invisible, antagonistic microbe of the dysentery bacillus". For d’Hérelle, there was no question as to the nature of his discovery: "In a flash I had understood: what caused my clear spots was in fact an invisible microbe … a virus parasitic on bacteria."[7] D'Hérelle called the virus a bacteriophage or bacteria-eater (from the Greek phagein meaning to eat). He also recorded a dramatic account of a man suffering from dysentery who was restored to good health by the bacteriophages.[8] It was D'Herelle who conducted much research into bacteriophages and introduced the concept of phage therapy.[9]

In 1969, Max Delbrück, Alfred Hershey and Salvador Luria were awarded the Nobel Prize in Physiology and Medicine for their discoveries of the replication of viruses and their genetic structure.[10]

Phage therapy
Main article: Phage therapy
Phages were discovered to be antibacterial agents and were used in the former Soviet Republic of Georgia (pioneered there by Giorgi Eliava with help from the co-discoverer of bacteriophages, Felix d'Herelle) and the United States during the 1920s and 1930s for treating bacterial infections. They had widespread use, including treatment of soldiers in the Red Army. However, they were abandoned for general use in the West for several reasons:

Medical trials were carried out, but a basic lack of understanding of phages made these invalid.[11]
Antibiotics were discovered and marketed widely. They were easier to make, store and to prescribe.
Former Soviet research continued, but publications were mainly in Russian or Georgian languages, and were unavailable internationally for many years.
Clinical trials evaluating the antibacterial efficacy of bacteriophage preparations were conducted without proper controls and were methodologically incomplete preventing the formulation of important conclusions.[citation needed]
Their use has continued since the end of the Cold War in Georgia and elsewhere in Central and Eastern Europe. Globalyz Biotech is an international joint venture that commercializes bacteriophage treatment and its various applications across the globe. The company has successfully used bacteriophages in administering Phage therapy to patients suffering from bacterial infections, including: Staphylococcus (including MRSA), Streptococcus, Pseudomonas, Salmonella, skin and soft tissue, gastrointestinal, respiratory, and orthopedic infections. In 1923, the Eliava Institute was opened in Tbilisi, Georgia, to research this new science and put it into practice.

The first regulated randomized, double blind clinical trial was reported in the Journal of Wound Care in June 2009, which evaluated the safety and efficacy of a bacteriophage cocktail to treat infected venous leg ulcers in human patients. The study was approved by the FDA as a Phase I clinical trial. Study results satisfactorily demonstrated safety of therapeutic application of bacteriophages, however it did not show efficacy. The authors explain that the use of certain chemicals that are part of standard wound care (e.g. lactoferrin, silver) may have interfered with bacteriophage viability. Another regulated clinical trial in Western Europe (treatment of ear infections caused by Pseudomonas aeruginosa) was reported shortly after in the journal Clinical Otolaryngology in August 2009.[14] The study concludes that bacteriophage preparations were safe and effective for treatment of chronic ear infections in humans. Additionally, there have been numerous animal and other experimental clinical trials evaluating the efficacy of bacteriophages for various diseases, such as infected burns and wounds, and cystic fibrosis associated lung infections, among others. Meanwhile, Western scientists are developing engineered viruses to overcome antibiotic resistance, and engineering the phage genes responsible for coding enzymes which degrade the biofilm matrix, phage structural proteins and also enzymes responsible for lysis of bacterial cell wall.[2][3][4]

D'Herelle "quickly learned that bacteriophages are found wherever bacteria thrive: in sewers, in rivers that catch waste runoff from pipes, and in the stools of convalescent patients."[12] This includes rivers traditionally thought to have healing powers, including India's Ganges River.[13]

Replication

Diagram of the DNA injection process
Bacteriophages may have a lytic cycle or a lysogenic cycle, and a few viruses are capable of carrying out both. With lytic phages such as the T4 phage, bacterial cells are broken open (lysed) and destroyed after immediate replication of the virion. As soon as the cell is destroyed, the phage progeny can find new hosts to infect. Lytic phages are more suitable for phage therapy. Some lytic phages undergo a phenomenon known as lysis inhibition, where completed phage progeny will not immediately lyse out of the cell if extracellular phage concentrations are high. This mechanism is not identical to that of temperate phage going dormant and is usually temporary.

In contrast, the lysogenic cycle does not result in immediate lysing of the host cell. Those phages able to undergo lysogeny are known as temperate phages. Their viral genome will integrate with host DNA and replicate along with it fairly harmlessly, or may even become established as a plasmid. The virus remains dormant until host conditions deteriorate, perhaps due to depletion of nutrients; then, the endogenous phages (known as prophages) become active. At this point they initiate the reproductive cycle, resulting in lysis of the host cell. As the lysogenic cycle allows the host cell to continue to survive and reproduce, the virus is reproduced in all of the cell’s offspring. An example of a bacteriophage known to follow the lysogenic cycle and the lytic cycle is the phage lambda of E. coli.[14]

Sometimes prophages may provide benefits to the host bacterium while they are dormant by adding new functions to the bacterial genome in a phenomenon called lysogenic conversion. Examples are the conversion of harmless strains of Corynebacterium diphtheriae or Vibrio cholerae by bacteriophages to highly virulent ones, which cause Diphtheria or cholera, respectively.[15][16] Strategies to combat certain bacterial infections by targeting these toxin-encoding prophages have been proposed.[17]

Attachment and penetration

In this electron micrograph of bacteriophages attached to a bacterial cell, the viruses are the size and shape of coliphage T1.
To enter a host cell, bacteriophages attach to specific receptors on the surface of bacteria, including lipopolysaccharides, teichoic acids, proteins, or even flagella. This specificity means a bacteriophage can infect only certain bacteria bearing receptors to which they can bind, which in turn determines the phage's host range. Host growth conditions also influence the ability of the phage to attach and invade them.[18] As phage virions do not move independently, they must rely on random encounters with the right receptors when in solution (blood, lymphatic circulation, irrigation, soil water, etc.).

Myovirus bacteriophages use a hypodermic syringe-like motion to inject their genetic material into the cell. After making contact with the appropriate receptor, the tail fibers flex to bring the base plate closer to the surface of the cell; this is known as reversible binding. Once attached completely, irreversible binding is initiated and the tail contracts, possibly with the help of ATP present in the tail,[3] injecting genetic material through the bacterial membrane. Podoviruses lack an elongated tail sheath similar to that of a myovirus, so they instead use their small, tooth-like tail fibers to enzymatically degrade a portion of the cell membrane before inserting their genetic material.

Synthesis of proteins and nucleic acid
Within minutes, bacterial ribosomes start translating viral mRNA into protein. For RNA-based phages, RNA replicase is synthesized early in the process. Proteins modify the bacterial RNA polymerase so it preferentially transcribes viral mRNA. The host’s normal synthesis of proteins and nucleic acids is disrupted, and it is forced to manufacture viral products instead. These products go on to become part of new virions within the cell, helper proteins that help assemble the new virions, or proteins involved in cell lysis. Walter Fiers (University of Ghent, Belgium) was the first to establish the complete nucleotide sequence of a gene (1972) and of the viral genome of bacteriophage MS2 (1976).[19]

Virion assemblyIn the case of the T4 phage, the construction of new virus particles involves the assistance of helper proteins. The base plates are assembled first, with the tails being built upon them afterwards. The head capsids, constructed separately, will spontaneously assemble with the tails. The DNA is packed efficiently within the heads. The whole process takes about 15 minutes.

Release of virions
Phages may be released via cell lysis, by extrusion, or, in a few cases, by budding. Lysis, by tailed phages, is achieved by an enzyme called endolysin, which attacks and breaks down the cell wall peptidoglycan. An altogether different phage type, the filamentous phages, make the host cell continually secrete new virus particles. Released virions are described as free, and, unless defective, are capable of infecting a new bacterium. Budding is associated with certain Mycoplasma phages. In contrast to virion release, phages displaying a lysogenic cycle do not kill the host but, rather, become long-term residents as prophage.

Genome structure
Bacteriophage genomes are especially mosaic: the genome of any one phage species appears to be composed of numerous individual modules. These modules may be found in other phage species in different arrangements. Mycobacteriophages – bacteriophages with mycobacterial hosts – have provided excellent examples of this mosaicism. In these mycobacteriophages, genetic assortment may be the result of repeated instances of site-specific recombination and illegitimate recombination (the result of phage genome acquisition of bacterial host genetic sequences).[20] It should be noted, however, that evolutionary mechanisms shaping the genomes of bacterial viruses vary between different families and depend on the type of the nucleic acid, characteristics of the virion structure, as well as the mode of the viral life cycle.[21]

In the environment
Main article: Marine bacteriophage
Metagenomics has allowed the in-water detection of bacteriophages that was not possible previously.[22]

Bacteriophages have also been used in hydrological tracing and modelling in river systems, especially where surface water and groundwater interactions occur. The use of phages is preferred to the more conventional dye marker because they are significantly less absorbed when passing through ground waters and they are readily detected at very low concentrations.[23]

Other areas of use
Since 2006, the United States Food and Drug Administration (FDA) and United States Department of Agriculture (USDA) have approved several bacteriophage products. LMP-102 (Intralytix) was approved for treating ready-to-eat (RTE) poultry and meat products. In that same year, the FDA approved LISTEX (developed and produced by Micreos) using bacteriophages on cheese to kill Listeria monocytogenes bacteria, giving them generally recognized as safe (GRAS) status.[24] In July 2007, the same bacteriophage were approved for use on all food products.[25] In 2011 USDA confirmed that LISTEX is a clean label processing-aid and is included in USDA.[26] Research in the field of food safety is continuing to see if lytic phages are a viable option to control other food-borne pathogens in various food products.

In 2011 the FDA cleared the first bacteriophage-based product for in vitro diagnostic use.[27] The KeyPath MRSA/MSSA Blood Culture Test uses a cocktail of bacteriophage to detect Staphylococcus aureus in positive blood cultures and determine methicillin resistance or susceptibility. The test returns results in about 5 hours, compared to 2–3 days for standard microbial identification and susceptibility test methods. It was the first accelerated antibiotic susceptibility test approved by the FDA.[28]

Government agencies in the West have for several years been looking to Georgia and the former Soviet Union for help with exploiting phages for counteracting bioweapons and toxins, such as anthrax and botulism.[29] Developments are continuing among research groups in the US. Other uses include spray application in horticulture for protecting plants and vegetable produce from decay and the spread of bacterial disease. Other applications for bacteriophages are as biocides for environmental surfaces, e.g., in hospitals, and as preventative treatments for catheters and medical devices prior to use in clinical settings. The technology for phages to be applied to dry surfaces, e.g., uniforms, curtains, or even sutures for surgery now exists. Clinical trials reported in the Lancet[30] show success in veterinary treatment of pet dogs with otitis.

Phage display is a different use of phages involving a library of phages with a variable peptide linked to a surface protein. Each phage's genome encodes the variant of the protein displayed on its surface (hence the name), providing a link between the peptide variant and its encoding gene. Variant phages from the library can be selected through their binding affinity to an immobilized molecule (e.g., botulism toxin) to neutralize it. The bound, selected phages can be multiplied by reinfecting a susceptible bacterial strain, thus allowing them to retrieve the peptides encoded in them for further study.[citation needed]

The SEPTIC bacterium sensing and identification method uses the ion emission and its dynamics during phage infection and offers high specificity and speed for detection.[citation needed]

Phage-ligand technology makes use of proteins, which are identified from bacteriophages, characterized and recombinantly expressed for various applications such as binding of bacteria and bacterial components (e.g. endotoxin) and lysis of bacteria.[31]

Bacteriophages are also important model organisms for studying principles of evolution and ecology.[32]

Model bacteriophages
The following bacteriophages are extensively studied:

λ phage
T2 phage
T4 phage (169 kbp genome,[33] 200 nm long[citation needed])
T7 phage
T12 phage
R17 phage
M13 phage
MS2 phage (23–25 nm in size[citation needed])
G4 phage
P1 phage
Enterobacteria phage P2
P4 phage
Phi X 174 phage
N4 phage
Pseudomonas phage Φ6
Φ29 phage
186 phage
Cultural references[edit]
In 1925 in the Pulitzer Prize-winning novel Arrowsmith, Sinclair Lewis fictionalized the discovery and application of bacteriophages as a therapeutic agent.
The 1999 Greg Bear novel Darwin's Radio deals with an epidemic in the form of long-dormant sections of human DNA, introduced in prehistoric times by lysogenic bacteriophages, which begin to express themselves. The sequel, Darwin's Children, takes place in the post-epidemic world.

References
^ Jump up to: a b Mc Grath S and van Sinderen D (editors). (2007). Bacteriophage: Genetics and Molecular Biology (1st ed.). Caister Academic Press. ISBN 978-1-904455-14-1. [1].
^ Jump up to: a b Wommack, K. E.; Colwell, R. R. (2000). "Virioplankton: Viruses in Aquatic Ecosystems". Microbiology and Molecular Biology Reviews 64 (1): 69–114. doi:10.1128/MMBR.64.1.69-114.2000. PMC 98987. PMID 10704475.
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[ecstatichamster]

I've had some success with S. Boulardii normalizing my health. I know some type 2 diabetics taking it who are doing better.

 

[narouz]

post 110561 I've had some success with S. Boulardii normalizing my health. I know some type 2 diabetics taking it who are doing better.

I made a lot of changes about half a year ago,
and I think I've narrowed it down to certain probiotics that have helped me most clearly.
And s. boulardii is one of them.

I've been experimenting with s. boulardii, l. rhamnosis, and b. coagulans, mostly.
Oh, also l. reuteri.
It's complicated
because I've been experimenting with using them alone, or in pairs, or all together, etc.

As I noted above,
one of or combinations of those probiotics has given me
a persistently clean, pink tongue for the first time in 2 or 3 years.
That is very gratifying.
Perhaps I shouldn't attach so much value to that, but...I do.
That coated tongue thing is a bummer,
and seemed to betoken other more widespread things going on in my gut.

Mine has not been a perfectly designed or controlled experiment,
but I've been pretty careful with this
and I'm pretty sure those probiotics are mainly responsible for me finally being able to dose up my NDT thyroid supps
without getting the heart palps, skips, racing--pretty severe.

My working hypothesis is that, post-antibiotics and post-appendix,
I developed a yeast/fungal/candida overgrowth.
I'm thinking that is maybe behind my NAFLD and high iron.
Gut inflamed.
Gut lining permeable.
Endotoxin galore.
Burden on the liver.
Liver causes palpitations....

I think I need to put the s. boulardii info over on the thread about
"Fixing the Liver Before Going Full Peat."
We've talked a lot about strategies to fix the liver over there,
but I don't think s. boulardii has been mentioned,
and there are studies showing benefits in this regard....

 

[ecstatichamster]

I made a lot of changes about half a year ago,
and I think I've narrowed it down to certain probiotics that have helped me most clearly.
And s. boulardii is one of them.

I've been experimenting with s. boulardii, l. rhamnosis, and b. coagulans, mostly.
Oh, also l. reuteri.
It's complicated
because I've been experimenting with using them alone, or in pairs, or all together, etc.

I take S. Boulardii washing it down with psyillium fiber. Along with soil based organisms (Prescript-Assist). Seems to really help a LOT. This makes it all kind of move down into the bowel as a mass, so it gets there more intact, in theory.

When you wipe your butt, it shouldn't soil the toilet paper. That's one of the tests for inflammation, and you pass if you don't soil the toilet paper.

Coated tongue is a classic overgrowth symptom.

 

[Parsifal]

Starches give me a white tongue (and if I avoid them my gut health is very good) and milk can also do it. Where you avoiding insoluble fibers in the first place narouz?

 

[lollipop]

I just saw this study on resistant starch and the assumption continues to be that it increases gut bacteria which is the mechanism for "healing"

https://www.sciencedaily.com/releases/2016/06/160630140905.htm

 

[Peater Piper]

I just saw this study on resistant starch and the assumption continues to be that it increases gut bacteria which is the mechanism for "healing"

https://www.sciencedaily.com/releases/2016/06/160630140905.htm

I don't think they're saying it increased the overall population of bacteria in the colon (though it may have), but that it improved the balance of the bacteria. There's plenty of studies showing SCFAs tighten gut junctions and protect against endotoxin while lowering inflammation. I don't know if it's better to have a mostly sterile gut, or one replete with SCFA producing bacteria, but it seems a little strange to write off SCFAs completely because they place additional burden on the liver. Long chain fatty acids and fructose both place a strain on the liver and under the right circumstances can cause NAFLD, but that doesn't mean natural sugars and saturated fat should be avoided by everyone.

 

[whodathunkit]

I lost over 50lbs when I was experimenting with resistant starch and a wide variety of probiotic strains last year. I don't think the bacteria or starch did much if anything to help me lose the weight, but they sure didn't hurt my efforts. Subjectively, they helped increase my energy and stamina.

For whatever that's worth.

 

[InterrogaOmnia]

It seems like at least once a week I go through this cycle where I get a massive all day migraine. I feel like I have tunnel vision and can't focus very well. My appetite dissappears and I get slight nauseous feelings off and on. Plus I get this weird almost have to sneeze but not really feeling. Digestion feels off. Poop becomes very acidic. I get some nasty bags under my eyes too. I've tried everything I can think of to stop the migraines but really nothing seems to help that much. Maybe magnesium would help? They seem to inevitably happen when I eat large amounts of starch for consecutive days. Pretty much without fail it seems. I even tried to limit my starch to amylopectin rice and without fail, eating too many bowls of rice screws me up pretty bad in the coming days. I've known starch was the culprit for a while now. But it really sucks, because I find little satisfaction eating a low or starch free diet. I've had issues with my bowels for as long as I can remember. And I surely have some bacterial issues. My tongue gets very coated with gunk during these events, and oddly I have a single tooth that starts aching at the root. Same tooth every time. Guess I really just need to decide between feeling like ***t or being less satisfied with my food.

 

[Bodhi]

" THE SMALL INTESTINE When food has passed through the stomach by way of the mouth and esophagus, it enters the long, coiled tube called the small intestine. Here is where about 90% of the absorption into the bloodstream of all food constituents takes place. By the time it reaches the small intestine, food from the mouth has been reduced by the action of chewing and digestive juices into a liquid known as “chyme.” Digestion of carbohydrates starts in the mouth with saliva. Further digestion takes place in the stomach. Proteins are broken down into short chains of amino acids (the essential ingredients of protein formation) in the stomach, while further reduction takes place in the small intestine until the molecules can be properly absorbed. When chyme has been thoroughly mixed and broken down by the stomach, the pyloric sphincter muscle valve opens and allows the food to enter into the uppermost portion of the small intestine or duodenum. Here in the duodenum, the first of three portions of the small intestine, the chyme is again thoroughly mixed by the contraction of the muscular walls. The longitudinal and circular muscles of the intestinal walls are capable of performing three different types of movements, each serving a different purpose. The tube of the small intestine is divided by the circular muscles. These contract, segmenting the food as it passes. Further contraction of the muscles between these segments occurs, making smaller segments, then the first set of muscles relax. This action results in a sloshing motion called rhythmic segmentation and takes place 12 to 16 times a minute. As a result of these movements, the chyme is thoroughly mixed with digestive juices. A wave of contraction known as peristalsis flows from the duodenum through the jejunum, or middle portion of the small intestine, all the way to and through the ileum, third and final portion. Peristalsis is the motion caused by the rhythmic coordination of the muscles and propels the chyme through the small intestine. Normal muscular activity of the intestine is not usually felt, although toxin-producing bacteria may cause violent and painful spasms to be felt. Diarrhea and vomiting are both reactions to irritations of the stomach and bowel.
THE SMALL INTESTINE
When food has passed through the stomach by way of the mouth and esophagus, it enters
the long, coiled tube called the small intestine. Here is where about 90% of the absorption into
the bloodstream of all food constituents takes place. By the time it reaches the small intestine,
food from the mouth has been reduced by the action of chewing and digestive juices into a liquid
known as “chyme.”
Digestion of carbohydrates starts in the mouth with saliva. Further digestion takes place in
the stomach. Proteins are broken down into short chains of amino acids (the essential ingredients
of protein formation) in the stomach, while further reduction takes place in the small intestine
until the molecules can be properly absorbed. When chyme has been thoroughly mixed and
broken down by the stomach, the pyloric sphincter muscle valve opens and allows the food to
enter into the uppermost portion of the small intestine or duodenum. Here in the duodenum, the
first of three portions of the small intestine, the chyme is again thoroughly mixed by the contraction
of the muscular walls.
The longitudinal and circular muscles of the intestinal walls are capable of performing three
different types of movements, each serving a different purpose. The tube of the small intestine is
divided by the circular muscles. These contract, segmenting the food as it passes. Further contraction
of the muscles between these segments occurs, making smaller segments, then the first
set of muscles relax. This action results in a sloshing motion called rhythmic segmentation and
takes place 12 to 16 times a minute. As a result of these movements, the chyme is thoroughly
mixed with digestive juices. A wave of contraction known as peristalsis flows from the duodenum
through the jejunum, or middle portion of the small intestine, all the way to and through the
ileum, third and final portion. Peristalsis is the motion caused by the rhythmic coordination of the
muscles and propels the chyme through the small intestine. Normal muscular activity of the intestine
is not usually felt, although toxin-producing bacteria may cause violent and painful spasms to
be felt. Diarrhea and vomiting are both reactions to irritations of the stomach and bowel"

"BACTERIAL ACTION IN THE BOWEL When the bowel is healthy there is very little bacterial action in the small intestine. The large intestine, however, lilterally swarms with billions of these microscopic organisms. Bacterial action in the large intestine plays a major role in nutrition and digestion. These friendly bacteria synthesize valuable nutrients by digesting portions of the fecal mass. Among others, vitamin K and portions of the B complex are produced. This aspect of digestion is not completely understood and is undergoing further study. Any remaining proteins are broken down by the bacteria into simpler substances. By products of bacterial activity are numerous, such as indole, skatole, hydrogen sulfide, fatty acids, methane gas and carbon dioxide. Some of these substances are very toxic and odorous, hence the accompanying smell of feces. The brown color of feces is a result of bile pigments coming from the liver. When feces are not brown, but have a chalky appearance, there is a problem in bile secretion and digestive ability. When feces reach the rectum they are about 70% water; 30% by weight of the mass represents bacteria while the remainder is made up of food residues, cellulose, indigestible materials and dead cells discarded by the body. The time it takes for chyme at the cecum to turn into feces and travel to the rectum depends upon the amount of roughage in the food and the water content. Bulkier feces travel faster as they provide substance for the bowel muscle to work upon. Otherwise a soft, fiberless stool becomes very difficult for the colon to move along. The longer it takes, the more water is absorbed, making feces compacted and hard so that it becomes difficult to eliminate them. Neglecting the urge to eliminate, as well as eating foods low in roughage, will lead to constipation. Laxatives, taken as an aid in elimination, either act to increase the amount of liquid retained in the feces, or act as a lubricant to allow for easy passage. Oftentimes laxatives are compounded to be an irritant or poison and stimulate the muscle walls to cause abnormal contractions to expel the irritating substances. It is very easy to become dependent upon these drugs and thereby permanently destroy normal bowel function. The expulsion of liquid feces or diarrhea, can be produced by excessive use of laxatives, nervous stress, infection or the presence of toxic substances in the bowel"

Expert from he book:

TISSUE CLEANSING THROUGH BOWEL MANAGEMENT By BERNARD JENSEN D.C., Nutritionist