Gut Bacteria Overgrowth, Regardless Of Type, Causes Obesity

Bodhi

Member
Joined
Mar 10, 2015
Messages
248
Age
47
Location
Netherlands
In 4 weeks i am gonna do another deep cleanse of my bowels in Thailand....
I love this type of detox originally you suppose not to eat on this cleanse while doing colonics..

I am gonna do it Peat style... keeping blood sugar up with coconut juice, fruits and fruit juices..
I am not gonna take the flora grow pro biotics, instead i ordered the Biosporin forte from Ukrain.
The one Peat refers to...

So sterile gut filled with B. subtilis and B. licheniformis....

See how that goes!
 

Mufasa

Member
Joined
Jun 10, 2016
Messages
624
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.
^ Jump up to: a b c Prescott, L. (1993). Microbiology, Wm. C. Brown Publishers, ISBN 0-697-01372-3
^ Jump up to: a b BBC Horizon (1997): The Virus that Cures – Documentary about the history of phage medicine in Russia and the West
Jump up ^ Keen, E. C. (2012). "Phage Therapy: Concept to Cure". Frontiers in Microbiology 3. doi:10.3389/fmicb.2012.00238. PMC 3400130. PMID 22833738.
Jump up ^ http://phys.org/news/2015-11-bacteria-b ... cally.html
Jump up ^ Félix d'Hérelles (1917). "Sur un microbe invisible antagoniste des bacilles dysentériques". Comptes rendus Acad Sci Paris. 165: 373–5. Archived from the original (PDF) on 4 December 2010. Retrieved 5 September 2010.
Jump up ^ Félix d'Hérelle (1949). "The bacteriophage" (PDF). Science News 14: 44–59. Retrieved 5 September 2010.
Jump up ^ Keen EC (2012). "Felix d’Herelle and Our Microbial Future". Future Microbiology 7 (12): 1337–1339. doi:10.2217/fmb.12.115. PMID 23231482.
Jump up ^ "The Nobel Prize in Physiology or Medicine 1969". Nobel Foundation. Retrieved 2007-07-28.
Jump up ^ Kutter, Elizabeth; De Vos, Daniel; Gvasalia, Guram; Alavidze, Zemphira; Gogokhia, Lasha; Kuhl, Sarah; Abedon, Stephen (1 January 2010). "Phage Therapy in Clinical Practice: Treatment of Human Infections". Current Pharmaceutical Biotechnology 11 (1): 69–86. doi:10.2174/138920110790725401. PMID 20214609.
Jump up ^ Kuchment, Anna (2012), The Forgotten Cure: The past and future of phage therapy, Springer, p. 11, ISBN 978-1-4614-0250-3
Jump up ^ Deresinski, Stan (15 April 2009). "Bacteriophage Therapy: Exploiting Smaller Fleas". Clinical Infectious Diseases 48 (8): 1096–1101. doi:10.1086/597405.
Jump up ^ Mason, Kenneth A., Jonathan B. Losos, Susan R. Singer, Peter H Raven, and George B. Johnson. (2011). Biology, p. 533. McGraw-Hill, New York. ISBN 978-0-07-893649-4.
Jump up ^ Mokrousov I (January 2009). "Corynebacterium diphtheriae: genome diversity, population structure and genotyping perspectives". Infection, Genetics and Evolution 9 (1): 1–15. doi:10.1016/j.meegid.2008.09.011. PMID 19007916.
Jump up ^ Charles RC, Ryan ET (October 2011). "Cholera in the 21st century". Current Opinion in Infectious Diseases 24 (5): 472–7. doi:10.1097/QCO.0b013e32834a88af. PMID 21799407.
Jump up ^ Keen, E. C. (December 2012). "Paradigms of pathogenesis: Targeting the mobile genetic elements of disease". Frontiers in Cellular and Infection Microbiology 2: 161. doi:10.3389/fcimb.2012.00161. PMC 3522046. PMID 23248780.
Jump up ^ Gabashvili, I.; Khan, S.; Hayes, S.; Serwer, P. (1997). "Polymorphism of bacteriophage T7". Journal of Molecular Biology 273 (3): 658–67. doi:10.1006/jmbi.1997.1353. PMID 9356254.
Jump up ^ Fiers, W.; Contreras, R.; Duerinck, F.; Haegeman, G.; Iserentant, D.; Merregaert, J.; Min Jou, W.; Molemans, F.; Raeymaekers, A.; Van Den Berghe, A.; Volckaert, G.; Ysebaert, M. (1976). "Complete nucleotide sequence of bacteriophage MS2 RNA: primary and secondary structure of the replicase gene". Nature 260 (5551): 500–507. Bibcode:1976Natur.260..500F. doi:10.1038/260500a0. PMID 1264203.
Jump up ^ Morris P, Marinelli LJ, Jacobs-Sera D, Hendrix RW, Hatfull GF (March 2008). "Genomic characterization of mycobacteriophage Giles: evidence for phage acquisition of host DNA by illegitimate recombination". Journal of Bacteriology 190 (6): 2172–82. doi:10.1128/JB.01657-07. PMC 2258872. PMID 18178732.
Jump up ^ Krupovic M, Prangishvili D, Hendrix RW, Bamford DH (December 2011). "Genomics of bacterial and archaeal viruses: dynamics within the prokaryotic virosphere". Microbiology and Molecular Biology Reviews : MMBR 75 (4): 610–35. doi:10.1128/MMBR.00011-11. PMC 3232739. PMID 22126996.
Jump up ^ Breitbart, M, P Salamon, B Andresen, J Mahaffy, A Segall, D Mead, F Azam, F Rohwer (2002) Genomic analysis of uncultured marine viral communities. Proceedings of the National Academy USA. 99:14250-14255.
Jump up ^ Martin, C. (1988). "The Application of Bacteriophage Tracer Techniques in South West Water". Water and Environment Journal 2: 638. doi:10.1111/j.1747-6593.1988.tb01352.x.
Jump up ^ U.S. FDA/CFSAN: Agency Response Letter, GRAS Notice No. 000198
Jump up ^ (U.S. FDA/CFSAN: Agency Response Letter, GRAS Notice No. 000218)
FSIS Directive 7120

The New York Times: Studying anthrax in a Soviet-era lab – with Western funding
Wright, A.; Hawkins, C.; Anggård, E.; Harper, D. (2009). "A controlled clinical trial of a therapeutic bacteriophage preparation in chronic otitis due to antibiotic-resistant Pseudomonas aeruginosa; a preliminary report of efficacy". Clinical Otolaryngology 34 (4): 349–357. doi:10.1111/j.1749-4486.2009.01973.x. PMID 19673983.
Technological background Phage-ligand technology
Keen, E. C. (2014). "Tradeoffs in bacteriophage life histories". Bacteriophage 4 (1): e28365. doi:10.4161/bact.28365. PMC 3942329. PMID 24616839.
Jump up ^ Miller, ES; Kutter, E; Mosig, G; Arisaka, F; Kunisawa, T; Rüger, W (March 2003). "Bacteriophage T4 genome.". Microbiology and molecular biology reviews : MMBR 67 (1): 86–156, table of contents. doi:10.1128/MMBR.67.1.86-156.2003. PMC 150520. PMID 12626685.

Narouz discovered bacteriophages before Ray Peat lol
 

charmer

Member
Joined
Oct 25, 2014
Messages
61
In 4 weeks i am gonna do another deep cleanse of my bowels in Thailand....
I love this type of detox originally you suppose not to eat on this cleanse while doing colonics..

I am gonna do it Peat style... keeping blood sugar up with coconut juice, fruits and fruit juices..
I am not gonna take the flora grow pro biotics, instead i ordered the Biosporin forte from Ukrain.
The one Peat refers to...

So sterile gut filled with B. subtilis and B. licheniformis....

See how that goes!
So how did it go?
 

Waynish

Member
Joined
Oct 11, 2016
Messages
2,206
It's pretty well established that "disease begins in the gut" is a useful generalization... However, gut healing protocols still have a lot to be desired from many people. I was on fairly high dose cyproheptadine recently - to no great avail. I enjoyed the increase in appetite, but it doesn't seem like it was enough to wipe out my SIBO (or whatever is bloating my small intestine).
 

charmer

Member
Joined
Oct 25, 2014
Messages
61
It's pretty well established that "disease begins in the gut" is a useful generalization... However, gut healing protocols still have a lot to be desired from many people. I was on fairly high dose cyproheptadine recently - to no great avail. I enjoyed the increase in appetite, but it doesn't seem like it was enough to wipe out my SIBO (or whatever is bloating my small intestine).
Cypro would probably have the opposite effect, because your intestine may be heavily reliant on serotonin to get things moving. So unless you are getting rid of bacteria, you might actually be prolonging the time toxins stay in your intestine. Cypro gave me restless legs because of this. So I wouldn't use it alone, definitely with cascara or somethings that stimulates excretion.
 

Amazoniac

Member
Joined
Sep 10, 2014
Messages
8,583
Location
Not Uganda
- The evolution of the host microbiome as an ecosystem on a leash

"At each body site, many different species and strains occur, each with the potential to interact with the host by modulating metabolism and the immune system that is itself a vastly complex biological system4. Moreover, each species has the potential to exert diverse effects on neighbouring microbes9. Some species kill others with dedicated toxins1012, while others invest in enzymes that feed other species for mutual benefit13."

"Many studies have focused on how the microbiota affects human health (microbe-to-host). However, here we argue that the other effects (host-to-microbe and microbe-to-microbe) explain why most functions evolve within the microbiome. Specifically, natural selection on the microbiota alone is not expected to make them beneficial to the host; rather, microbiota evolution is dominated by the need for each species to compete and persist within the host9. However, at the same time hosts are under strong natural selection to shape their microbiota to be beneficial. Thus, rather than being intrinsically helpful, the microbiome is a dynamic microbial ecosystem held on an ever-evolving leash by the host (Fig. 2)."

"We first consider the evolutionary origins of the best-studied aspect of the microbiome, the beneficial effects of the microbes on the host. Interactions between hosts and their microbiota appear to include many examples of biological mutualism: interactions that provide fitness benefits to all the species involved18. However, a degree of caution is required; although benefits to the host have been well documented, it is difficult to show that microbes benefit, because we typically do not know if better alternatives exist for microbes outside of the host19. If microbes do not benefit, the prediction is that natural selection will favour strategies to escape from the microbiome, or adaptions that increase within-host fitness, even if this harms the host. Nevertheless, for many species in environments like the human gut, the combination of relatively stable conditions, nutrients and warmth is likely to improve microbial fitness relative to host-free environments."

"For microbes that benefit from living inside a host, it might seem inevitable that natural selection would favour the evolution of microbe-to-host benefits. Evolutionary theory, however, shows otherwise. Consider a bacterial strain that generates a nutrient for the host, but must divide more slowly to do so. If this is the only strain within the host, then it can persist and continue to help its host, as this slow-growing strain will have no microbial competitors. However, in a diverse microbiota, the slow-growing strain runs the risk of being outcompeted by other faster-growing genotypes that do not make the nutrient (Box 2, Box 2 Figure). As a result, natural selection is predicted to favour microbes that invest in their own reproduction, rather than help the host2022."

"Crucially then, we cannot assume that the host and microbiota are a single evolutionary unit acting with a common interest, as is sometimes done in applications of the ‘holobiont’ or ‘superorganism’ metaphors23 (although see ref. 24). Rather, the host and each individual microbial strain are distinct entities with potentially divergent selective pressures."

"While hosts may have evolved multiple means to regulate their microbiota, the control of all strains in a community is challenging and—in the face of vast microbial diversity—probably impossible. Thus, which microbial species persist will not only depend on host control, but also on their ability to compete in the microbiome jungle58."

"A key determinant of biological function is resource competition (Box 1). Host diet has a major impact on the available resources within animals and, accordingly, which microbial species and types of metabolism can dominate59. Resources may also come from a host’s attempts to exert control, such as through mucin secretion22,52. Competition over resources in an evolving microbial population can drive rapid evolutionary radiations where different strains diverge into different niches to reduce competition (character displacement)60,61. Notably, this suggests that we each carry strains that are tuned to our specific set of niches, which may in turn promote colonization resistance by ensuring that invading strains are less evolutionarily adapted. Availability of a resource to exploit, however, is not sufficient for persistence. Microbial cells influence each other in many ways9, and these interactions can determine whether any given strain can persist6 and, more generally, which traits are needed to compete in a given community62."

"Microbes use diverse mechanisms to compete with other members of the microbiota6,62. This includes resource acquisition as discussed [], but also physical properties such as adhesiveness63, production of antibiotics and bacteriocins11, and toxic effector proteins delivered by the spear-like type-VI secretion system10,12. These activities eliminate competitors and contribute to determining which strains persist in the gut10,11. More subtle competition occurs by monitoring and manipulating signalling molecules of competitors, which appears to occur for the quorum-sensing molecule autoinducer-2 (AI-2)64. Bacteriophages (or phages) are also abundant in the gut65 and can impact microbial competition and promote diversity; phages tend to spread easily through host bacteria that are plentiful, which can give rarer species an advantage14. Finally, phages drive horizontal gene transfer (HGT). The evolutionary impacts of HGT, by phage and other means, is an important area of microbiome research. Even when rare, HGT can have major effects66,67 and move a single function, such as antibiotic resistance, horizontally through competing strains and species66."

"Many microbes also employ cooperative traits to remain competitive within communities. Cells secrete enzymes that degrade complex molecules, siderophores that scavenge iron, and quorum-sensing molecules that function as a communication system to report on cell density, diffusion conditions and genetic mixing9. In vitro and genomic studies indicate that host-associated microbes exhibit many of these phenotypes68,69, but inferring the function of extracellular enzymes can be challenging. Bacteroides thetaiotaomicron, an abundant species in the human gut microbiome, carries extracellular enzymes that degrade complex carbohydrates. However, the import of breakdown products is so effective that few products are actually shared with others, which renders carbohydrate breakdown by this species a largely private function13,70."

"Indeed, the evolution of microbial cooperation is only expected under certain conditions. Genotypes that benefit from cooperative traits, but do not provide them (sometimes called ‘cheaters’) can invade cooperating populations and replace them, rendering cooperation unstable."

"How do the diverse microbial functions we have discussed combine at the level of the whole microbiome, and what is the effect on the host? Ecological theory provides a map between the properties of individual species and the properties of the whole community1,14. The mammalian microbiota often responds robustly to perturbations, allowing a host to keep key species for long periods75,76. Theory suggests that the key to this stability lies in how species interact with one another. Weak and competitive interactions are stabilizing14—they limit positive feedback loops and the possibility that, if one species goes down, it will take others with it. Another key property is productivity, that is the efficiency of converting resources into energy. In this case, it is cooperative interactions that can improve a community by preventing wasteful functions such as antibiotic competition9. A host may then face a tension between communities that are highly productive and those that are stable14."

"Another community-level property is redundancy: the coexistence of species with a similar impact on the ecosystem. Redundancy may benefit a host, because other microbes can then compensate for the loss of a beneficial strain by providing the same benefit."

"The importance of host control does not imply that community composition will remain static. Omnivorous hosts, in particular, may benefit from a flexible microbiota that can respond to changing metabolic demands. The fact that microbiome communities can shift strongly with host diet59, therefore, is not in itself evidence that a host is powerless to influence communities. Indeed, humans display a remarkable ability to keep major microbial lineages within our microbiota75,76, to the extent that several bacterial lineages appear to have co-speciated with us88. As for many other hosts, this suggests that humans have evolved to create an environment that selects for specific bacterial lineages. Strong perturbations, however, may force a host to deal with extinctions, followed by stochastic recolonization as new species arrive at random. This potential for recolonization is expected to promote trait-based discrimination in a host (see ‘Monitoring and targeting’), which applies general selection for microbes based on their benefits rather than targeting specific genotypes. As a corollary, hosts may be sometimes blind to an immigrating strain outcompeting a resident, so long as the new strain has the equivalent effect on a host."

"Certainly, evolutionary theory does not predict that each symbiont strain will provide a benefit, unique or otherwise, but it does predict that all strains will be effective competitors (Boxes 1 and 2)."

"[..]even if a species provides no direct benefit to the host, it may contribute to overall community stability[.]"

"If a host already has ways to regulate the microbiota, augmenting these mechanisms offers an alternative to targeting the microbes themselves."​
 
Last edited:

Amazoniac

Member
Joined
Sep 10, 2014
Messages
8,583
Location
Not Uganda
- Esophagus - Wikipedia
- Stomach - Wikipedia (missing)
- Small intestine - Wikipedia
- Large intestine - Wikipedia

upload_2020-1-13_21-33-33.png
 

tankasnowgod

Member
Joined
Jan 25, 2014
Messages
8,131
Taking antibiotics in infancy is also associated with obesity. Strange no?

Not really, in fact, it's likely perfectly in line with the original study. Antibiotics aren't just given out willy nilly. They are prescribed due to some infection. Most in the alterna-health sphere have interpreted this as the antibiotics causing disregulation (a possibility), but it's just as likely that the antibiotics were prescribed for some sort of overgrowth, and that persisted into adulthood, or that person was less likely to be able to to keep bacteria in check due to a compromised immune system or something.

And yes, I realize this comment is 4+ years old, but this thread popped up again.
 
Last edited:

Matestube

Member
Joined
Dec 28, 2021
Messages
912
Location
Dubai
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.

I had the same exact symptoms once a week.
I cured it with completely eliminating starches and fiber and getting at least five cups of coffee a day.

Also take Epsom salts (or magnesium citrate if that's what you have access to) once a week to completely flush your gut clean.
 

Similar threads

Back
Top Bottom