4029 replies to this topic

[Mr Matsubayashi]

I just bought a bottle of this stuff from amazon:

http://www.amazon.co...0?ie=UTF8&psc=1

Started adding a tbsp of potato starch to my morning soylent.

http://quackfiles.bl...cs-warning.html

[lostfalco]

I just bought a bottle of this stuff from amazon:

http://www.amazon.co...0?ie=UTF8&psc=1

Started adding a tbsp of potato starch to my morning soylent.

http://quackfiles.bl...cs-warning.html

Just to clarify...I'm recommending PREbiotics first. Prebiotics = food for good bacteria. Probiotics = good bacteria themselves. I think that most people already have the good bacteria, they just need to feed them (obviously, there will be exceptions). In most cases, probiotics are probably unnecessary. =)

I'll post abstracts to all of the 2014 studies that I'm currently going through in another post. Give me just one minute....

[Nattzor]

Just to clarify...I'm recommending PREbiotics first. Prebiotics = food for good bacteria. Probiotics = good bacteria themselves. I think that most people already have the good bacteria, they just need to feed them (obviously, there will be exceptions). In most cases, probiotics are probably unnecessary. =)

I'll post abstracts to all of the 2014 studies that I'm currently going through in another post. Give me just one minute....

I'd recommend both instead. There is tons of research on individual strains (everything from making rats "glow" of health/beauty, curing Crohn's (well, that's mainly poop) to less bodyfat and better blood profiles), probiotic meals (kefir, sauerkraut, etc), all showing vert promising results. I'm guessing, due to the hygiene standards we have today, we've fucked up most of the bacterias we have. Introducing more ("good") strains when also adding prebiotics to help them, and the others, survive will most likely produce the best results.

[lostfalco]

Abstracts and more abstracts...Enjoy! (sorry about the obnoxiously long post, I know that pretty much everybody knows how to use pubmed =))

http://www.ncbi.nlm....pubmed/24412651

Cell. 2014 Jan 16;156(1-2):84-96. doi: 10.1016/j.cell.2013.12.016. Epub 2014 Jan 9.

Microbiota-Generated Metabolites Promote Metabolic Benefits via Gut-Brain Neural Circuits.

De Vadder F¹, Kovatcheva-Datchary P², Goncalves D¹, Vinera J¹, Zitoun C¹, Duchampt A¹, Bäckhed F³, Mithieux G⁴.

Author information
Abstract

Soluble dietary fibers promote metabolic benefits on body weight and glucose control, but underlying mechanisms are poorly understood. Recent evidence indicates that intestinal gluconeogenesis (IGN) has beneficial effects on glucose and energy homeostasis. Here, we show that the short-chain fatty acids (SCFAs) propionate and butyrate, which are generated by fermentation of soluble fiber by the gut microbiota, activate IGN viacomplementary mechanisms. Butyrate activates IGN gene expression through a cAMP-dependent mechanism, while propionate, itself a substrate of IGN, activates IGN gene expression via a gut-brain neural circuit involving the fatty acid receptor FFAR3. The metabolic benefits on body weight and glucose control induced by SCFAs or dietary fiber in normal mice are absent in mice deficient for IGN, despite similar modifications in gut microbiota composition. Thus, the regulation of IGN is necessary for the metabolic benefits associated with SCFAs and soluble fiber.

http://www.ncbi.nlm....pubmed/24388214
Adv Immunol. 2014;121:91-119. doi: 10.1016/B978-0-12-800100-4.00003-9.
The role of short-chain Fatty acids in health and disease.
Tan J1, McKenzie C1, Potamitis M1, Thorburn AN1, Mackay CR2, Macia L3.
Author information
Abstract
There is now an abundance of evidence to show that short-chain fatty acids (SCFAs) play an important role in the maintenance of health and the development of disease. SCFAs are a subset of fatty acids that are produced by the gut microbiota during the fermentation of partially and nondigestible polysaccharides. The highest levels of SCFAs are found in the proximal colon, where they are used locally by enterocytes or transported across the gut epithelium into the bloodstream. Two major SCFA signaling mechanisms have been identified, inhibition of histone deacetylases (HDACs) and activation of G-protein-coupled receptors (GPCRs). Since HDACs regulate gene expression, inhibition of HDACs has a vast array of downstream consequences. Our understanding of SCFA-mediated inhibition of HDACs is still in its infancy. GPCRs, particularly GPR43, GPR41, and GPR109A, have been identified as receptors for SCFAs. Studies have implicated a major role for these GPCRs in the regulation of metabolism, inflammation, and disease. SCFAs have been shown to alter chemotaxis and phagocytosis; induce reactive oxygen species (ROS); change cell proliferation and function; have anti-inflammatory, antitumorigenic, and antimicrobial effects; and alter gut integrity. These findings highlight the role of SCFAs as a major player in maintenance of gut and immune homeostasis. Given the vast effects of SCFAs, and that their levels are regulated by diet, they provide a new basis to explain the increased prevalence of inflammatory disease in Westernized countries, as highlighted in this chapter.

http://www.ncbi.nlm....pubmed/24286462
Genes Brain Behav. 2014 Jan;13(1):69-86. doi: 10.1111/gbb.12109. Epub 2013 Dec 27.
Microbial genes, brain & behaviour - epigenetic regulation of the gut-brain axis.
Stilling RM, Dinan TG, Cryan JF.
Author information
Abstract
To date, there is rapidly increasing evidence for host-microbe interaction at virtually all levels of complexity, ranging from direct cell-to-cell communication to extensive systemic signalling, and involving various organs and organ systems, including the central nervous system. As such, the discovery that differential microbial composition is associated with alterations in behaviour and cognition has significantly contributed to establishing the microbiota-gut-brain axis as an extension of the well-accepted gut-brain axis concept. Many efforts have been focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome to neurodevelopmental disorders such as autism. There is also a growing appreciation of the role of epigenetic mechanisms in shaping brain and behaviour. However, the role of epigenetics in informing host-microbe interactions has received little attention to date. This is despite the fact that there are many plausible routes of interaction between epigenetic mechanisms and the host-microbiota dialogue. From this new perspective we put forward novel, yet testable, hypotheses. Firstly, we suggest that gut-microbial products can affect chromatin plasticity within their host's brain that in turn leads to changes in neuronal transcription and eventually alters host behaviour. Secondly, we argue that the microbiota is an important mediator of gene-environment interactions. Finally, we reason that the microbiota itself may be viewed as an epigenetic entity. In conclusion, the fields of (neuro)epigenetics and microbiology are converging at many levels and more interdisciplinary studies are necessary to unravel the full range of this interaction.

http://www.ncbi.nlm....pubmed/24332563
Med Hypotheses. 2014 Feb;82(2):163-6. doi: 10.1016/j.mehy.2013.11.026. Epub 2013 Dec 1.
Obsessive-compulsive disorder and gut microbiota dysregulation.
Rees JC.
Author information
Abstract
Obsessive-compulsive disorder (OCD) is a debilitating disorder for which the cause is not known and treatment options are modestly beneficial. A hypothesis is presented wherein the root cause of OCD is proposed to be a dysfunction of the gut microbiome constituency resulting in a susceptibility to obsessional thinking. Both stress and antibiotics are proposed as mechanisms by which gut microbiota are altered preceding the onset of OCD symptomology. In this light, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) leading to episodic OCD is explained not by group A beta-hemolytic streptococcal infections, but rather by prophylactic antibiotics that are administered as treatment. Further, stressful life events known to trigger OCD, such as pregnancy, are recast to show the possibility of altering gut microbiota prior to onset of OCD symptoms. Suggested treatment for OCD would be the directed, specie-specific (re)introduction of beneficial bacteria modifying the gut microbiome, thereby ameliorating OCD symptoms. Special considerations should be contemplated when considering efficacy of treatment, particularly the unhealthy coping strategies often observed in patients with chronic OCD that may need addressing in conjunction with microbiome remediation.

http://www.ncbi.nlm....pubmed/23516017
Cell Mol Life Sci. 2014 Jan;71(2):183-203. doi: 10.1007/s00018-013-1318-0. Epub 2013 Mar 21.
Molecular dialogue between the human gut microbiota and the host: a Lactobacillus and Bifidobacterium perspective.
Turroni F, Ventura M, Buttó LF, Duranti S, O'Toole PW, Motherway MO, van Sinderen D.
Author information
Abstract
The human gut represents a highly complex ecosystem, which is densely colonized by a myriad of microorganisms that influence the physiology, immune function and health status of the host. Among the many members of the human gut microbiota, there are microorganisms that have co-evolved with their host and that are believed to exert health-promoting or probiotic effects. Probiotic bacteria isolated from the gut and other environments are commercially exploited, and although there is a growing list of health benefits provided by the consumption of such probiotics, their precise mechanisms of action have essentially remained elusive. Genomics approaches have provided exciting new opportunities for the identification of probiotic effector molecules that elicit specific responses to influence the physiology and immune function of their human host. In this review, we describe the current understanding of the intriguing relationships that exist between the human gut and key members of the gut microbiota such as bifidobacteria and lactobacilli, discussed here as prototypical groups of probiotic microorganisms.

http://www.ncbi.nlm....pubmed/23688247
Crit Rev Microbiol. 2014 Aug;40(3):273-80. doi: 10.3109/1040841X.2013.787043. Epub 2013 May 21.
Friendly pathogens: prevent or provoke autoimmunity.
Sathyabama S, Khan N, Agrewala JN.
Author information
Abstract
Abstract The gut microflora is an immense health asset for human beings. The mammalian gut harbors trillions of commensals. These microbes not only modulate local but also systemic immunity. Recently, various reports are evolving, which signify that the gut microbes can modulate, tune and tame the host immune response. Consequently, it advocates the significance of the microbial composition. Further, the microbiota provides a fine equilibrium to host by regulating immune homeostasis. Furthermore, disturbance in this population can incite imbalance in immune system, leading to molecular mimicry and therefore autoimmunity. Hence, it is imperative to understand the influence of these bugs in preventing or provoking immune system against the self-components. In this article, we highlight the interaction between different gut microbes and cells of immune system and the mechanism involved in controlling and curtailing various autoimmune diseases.

http://www.ncbi.nlm....pubmed/24390308

Nat Med. 2014 Jan 5. doi: 10.1038/nm.3444. [Epub ahead of print]

Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis.

Trompette A1, Gollwitzer ES1, Yadava K1, Sichelstiel AK1, Sprenger N2, Ngom-Bru C2, Blanchard C2, Junt T3, Nicod LP1, Harris NL4, Marsland BJ1.

Author information

Abstract

Metabolites from intestinal microbiota are key determinants of host-microbe mutualism and, consequently, the health or disease of the intestinal tract. However, whether such host-microbe crosstalk influences inflammation in peripheral tissues, such as the lung, is poorly understood. We found that dietary fermentable fiber content changed the composition of the gut and lung microbiota, in particular by altering the ratio of Firmicutes to Bacteroidetes. The gut microbiota metabolized the fiber, consequently increasing the concentration of circulating short-chain fatty acids (SCFAs). Mice fed a high-fiber diet had increased circulating levels of SCFAs and were protected against allergic inflammation in the lung, whereas a low-fiber diet decreased levels of SCFAs and increased allergic airway disease. Treatment of mice with the SCFA propionate led to alterations in bone marrow hematopoiesis that were characterized by enhanced generation of macrophage and dendritic cell (DC) precursors and subsequent seeding of the lungs by DCs with high phagocytic capacity but an impaired ability to promote T helper type 2 (TH2) cell effector function. The effects of propionate on allergic inflammation were dependent on G protein-coupled receptor 41 (GPR41, also called free fatty acid receptor 3 or FFAR3), but not GPR43 (also called free fatty acid receptor 2 or FFAR2). Our results show that dietary fermentable fiber and SCFAs can shape the immunological environment in the lung and influence the severity of allergic inflammation.

http://www.ncbi.nlm....pubmed/23703735
Hepatology. 2014 Jan;59(1):328-39. doi: 10.1002/hep.26494. Epub 2013 Nov 15.
Microbiota-liver axis in hepatic disease.
Chassaing B, Etienne-Mesmin L, Gewirtz AT.
Author information
Abstract
Accumulating evidence indicates that the gut microbiota, long appreciated to be a key determinant of intestinal inflammation, is also playing a key role in chronic inflammatory disease of the liver. Such studies have yielded a general central hypothesis whereby microbiota products activate the innate immune system to drive proinflammatory gene expression, thus promoting chronic inflammatory disease of the liver. This article reviews the background supporting this hypothesis, outlines how it can potentially explain classic and newly emerging epidemiological chronic inflammatory liver disease, and discusses potential therapeutic means to manipulate the microbiota so as to prevent and/or treat liver disease. (Hepatology 2014;58:328-339).

http://www.ncbi.nlm....pubmed/23740189
Gut. 2014 Jan;63(1):5-6. doi: 10.1136/gutjnl-2013-304969. Epub 2013 Jun 5.
Western lifestyle: a 'master' manipulator of the intestinal microbiota?
Hold GL.
KEYWORDS:
Diet, Intestinal microbiota

http://www.ncbi.nlm....pubmed/23909466
FEMS Microbiol Ecol. 2014 Jan;87(1):30-40. doi: 10.1111/1574-6941.12186. Epub 2013 Aug 28.
Prebiotic stimulation of human colonic butyrate-producing bacteria and bifidobacteria, in vitro.
Scott KP, Martin JC, Duncan SH, Flint HJ.
Author information
Abstract
Dietary macronutrients affect the composition of the gut microbiota, and prebiotics are used to improve and maintain a healthy gut. The impact of prebiotics on dominant gut bacteria other than bifidobacteria, however, is under-researched. Here, we report carbohydrate utilisation patterns for representative butyrate-producing anaerobes, belonging to the Gram-positive Firmicutes families Lachnospiraceae and Ruminococcaceae, by comparison with selected Bacteroides and Bifidobacterium species. Growth assessments using anaerobic Hungate tubes and a new rapid microtitre plate assay were generally in good agreement. The Bacteroides strains tested showed some growth on basal medium with no added carbohydrates, utilising peptides in the growth medium. The butyrate-producing strains exhibited different growth profiles on the substrates, which included starch, inulin, fructooligosaccharides (FOS), galactooligosaccharides (GOS) and xylooligosaccharides (XOS). Eleven were able to grow on short-chain FOS, but this number decreased as the chain length of the fructan substrates increased. Long-chain inulin was utilised by Roseburia inulinivorans, but by none of the Bifidobacterium species examined here. XOS was a more selective growth substrate than FOS, with only six of the 11 Firmicutes strains able to use XOS for growth. These results illustrate the selectivity of different prebiotics and help to explain why some are butyrogenic.
© 2013 Federation of European Microbiological Societies. Published by John Wiley & Sons Ltd. All rights reserved.

http://www.ncbi.nlm....pubmed/23909489
FEMS Microbiol Ecol. 2014 Jan;87(1):41-51. doi: 10.1111/1574-6941.12187. Epub 2013 Aug 23.
Impact of galacto-oligosaccharides on the gut microbiota composition and metabolic activity upon antibiotic treatment during in vitro fermentation.
Ladirat SE, Schuren FH, Schoterman MH, Nauta A, Gruppen H, Schols HA.
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Abstract
Prebiotics are considered to have potential to reduce disturbances in the gut microbiota induced by antibiotics. Results in literature are, however, not consistent. The current in vitro study conducted in a fermentation screening platform allowed to unambiguously compare the impact of galacto-oligosaccharides (GOS) on adult gut microbiota composition and activity upon treatment with four antibiotics at two doses. The changes in relative abundance of bacteria upon antibiotic treatment and the growth of Bifidobacterium and Lactobacillus upon GOS addition were antibiotic and dose dependant. This conclusion explains discrepancies in literature and indicates that particular combinations of GOS antibiotic should be studied. The combination GOS-Amoxicillin was especially of interest as, after decrease in Bifidobacterium levels, a recovery of mainly Bifidobacterium longum was observed and could be correlated with specific degradation patterns of GOS. Next to different degradation profiles of individual GOS, an accumulation of monosaccharides and intermediate organic acids was observed in antibiotic-treated microbiota as compared to nontreated microbiota. This showed that although GOS were utilized and beneficial bacteria could grow in 3 of 4 antibiotics tested, the metabolic activity of an antibiotic-treated microbiota was still disturbed as compared to the nontreated microbiota.

http://www.ncbi.nlm....pubmed/23829297
J Gastroenterol Hepatol. 2014 Jan;29(1):52-9. doi: 10.1111/jgh.12322.
Effect of multispecies probiotics on irritable bowel syndrome: A randomized, double-blind, placebo-controlled trial.
Yoon JS, Sohn W, Lee OY, Lee SP, Lee KN, Jun DW, Lee HL, Yoon BC, Choi HS, Chung WS, Seo JG.
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Abstract
BACKGROUND AND AIM:
The efficacy of treatment with multispecies probiotics on irritable bowel syndrome (IBS) symptoms and the alterations of gut microbiota in patients who have taken probiotics were investigated.
METHODS:
This randomized, double-blind, placebo-controlled trial involved 49 IBS patients (probiotics: 25, placebo: 24) diagnosed according to the Rome III criteria. Patients were randomly assigned to two groups: either to receive multispecies probiotics (a mixture of Bifidobacterium longum, B. bifidum, B. lactis, Lactobacillus acidophilus, L. rhamnosus, and Streptococcus thermophilus) twice a day for 4 weeks or to receive a placebo twice a day for 4 weeks. The primary efficacy end-point was the proportion of participants whose IBS symptoms were substantially relieved at week 4. Secondary end-points were the intensity of abdominal pain/discomfort, bloating, stool frequency/consistency, alterations in fecal microflora over the 4 weeks. Fecal microflora were analyzed in 34 patients (probiotics: 17, placebo: 17) by quantitative real-time polymerase chain reaction assays.
RESULTS:
The proportion of patients whose IBS symptoms were substantially relieved at week 4 was significantly higher in the probiotics group than in the placebo group: 68.0% (17/25) versus 37.5% (9/24) (P < 0.05). Secondary end-points such as improvement in abdominal pain/discomfort and bloating occurred in the probiotics group but not in the placebo group. Fecal analysis revealed that B. lactis, L. rhamnosus, and S. thermophilus had increased significantly in the probiotics group after 4 weeks and that B. lactis had increased in the placebo group.
CONCLUSIONS:
Multispecies probiotics are effective in IBS patients and induce the alterations in the composition of intestinal microbiota.

http://www.ncbi.nlm....pubmed/23941288
Int J Food Sci Nutr. 2014 Feb;65(1):79-88. doi: 10.3109/09637486.2013.825700. Epub 2013 Aug 13.
In vitro batch cultures of gut microbiota from healthy and ulcerative colitis (UC) subjects suggest that sulphate-reducing bacteria levels are raised in UC and by a protein-rich diet.
Khalil NA, Walton GE, Gibson GR, Tuohy KM, Andrews SC.
Author information
Abstract
Abstract Imbalances in gut microbiota composition during ulcerative colitis (UC) indicate a role for the microbiota in propagating the disorder. Such effects were investigated using in vitro batch cultures (with/without mucin, peptone or starch) inoculated with faecal slurries from healthy or UC patients; the growth of five bacterial groups was monitored along with short-chain fatty acid (SCFA) production. Healthy cultures gave two-fold higher growth and SCFA levels with up to ten-fold higher butyrate production. Starch gave the highest growth and SCFA production (particularly butyrate), indicating starch-enhanced saccharolytic activity. Sulphate-reducing bacteria (SRB) were the predominant bacterial group (of five examined) for UC inocula whereas they were the minority group for the healthy inocula. Furthermore, SRB growth was stimulated by peptone presumably due to the presence of sulphur-rich amino acids. The results suggest raised SRB levels in UC, which could contribute to the condition through release of toxic sulphide.

http://www.ncbi.nlm....pubmed/24322902
Nat Rev Gastroenterol Hepatol. 2014 Jan;11(1):1. doi: 10.1038/nrgastro.2013.238. Epub 2013 Dec 10.
Gut microbiota: Anti-cancer therapies affected by gut microbiota.
Greenhill C.

http://www.ncbi.nlm....pubmed/24296462
Curr Opin Endocrinol Diabetes Obes. 2014 Feb;21(1):15-21. doi: 10.1097/MED.0000000000000032.
Irritable bowel syndrome, inflammatory bowel disease and the microbiome.
Major G, Spiller R.
Author information
Abstract
PURPOSE OF REVIEW:
The review aims to update the reader on current developments in our understanding of how the gut microbiota impact on inflammatory bowel disease and the irritable bowel syndrome. It will also consider current efforts to modulate the microbiota for therapeutic effect.
RECENT FINDINGS:
Gene polymorphisms associated with inflammatory bowel disease increasingly suggest that interaction with the microbiota drives pathogenesis. This may be through modulation of the immune response, mucosal permeability or the products of microbial metabolism. Similar findings in irritable bowel syndrome have reinforced the role of gut-specific factors in this 'functional' disorder. Metagenomic analysis has identified alterations in pathways and interactions with the ecosystem of the microbiome that may not be recognized by taxonomic description alone, particularly in carbohydrate metabolism. Treatments targeted at the microbial stimulus with antibiotics, probiotics or prebiotics have all progressed in the past year. Studies on the long-term effects of treatment on the microbiome suggest that dietary intervention may be needed for prolonged efficacy.
SUMMARY:
The microbiome represents 'the other genome', and to appreciate its role in health and disease will be as challenging as with our own genome. Intestinal diseases occur at the front line of our interaction with the microbiome and their future treatment will be shaped as we unravel our relationship with it.

http://www.ncbi.nlm....pubmed/24287935
Appl Microbiol Biotechnol. 2014 Jan;98(2):563-77. doi: 10.1007/s00253-013-5405-9. Epub 2013 Nov 28.
Bifidobacteria: their impact on gut microbiota composition and their applications as probiotics in infants.
Di Gioia D, Aloisio I, Mazzola G, Biavati B.
Author information
Abstract
This review is aimed at describing the most recent advances in the gut microbiota composition of newborns and infants with a particular emphasis on bifidobacteria. The newborn gut microbiota is quite unstable, whereas after weaning, it becomes more stable and gets closer to the typical adult microbiota. The newborn and infant gut microbiota composition is impaired in several enteric and non-enteric pathologies. The core of this review is the description of the most recent documented applications of bifidobacteria to newborns and infants for their prevention and treatment. Acute diarrhea is the most studied disease for which bifidobacteria are applied with great success, Bifidobacterium longum and Bifidobacterium breve being the most applied species. Moreover, the most recent updates in the use of bifidobacteria for the prevention and treatment of pathologies typical of newborns, such as necrotizing enterocolitis, colics, and streptococcal infections, are presented. In addition, a number of not strictly enteric pathologies have in recent years evidenced a strict correlation with an aberrant gut microbiota in infants, in particular showing a reduced level of bifidobacteria. These diseases represent new potential opportunities for probiotic applications. Among them, allergic diseases, celiac disease, obesity, and neurologic diseases are described in this review. The preliminary use of bifidobacteria in in vitro systems and animal models is summarized as well as preliminary in vivo studies. Only after validation of the results via human clinical trials will the potentiality of bifidobacteria in the prevention and cure of these pathologies be definitely assessed.

http://www.ncbi.nlm....pubmed/24274865
Clin Liver Dis. 2014 Feb;18(1):59-71. doi: 10.1016/j.cld.2013.09.002. Epub 2013 Oct 24.
Obesity and NAFLD: The role of bacteria and microbiota.
Duseja A, Chawla YK.
Author information
Abstract
There are trillions of microorganisms in the human intestine collectively called gut microbiota. Obesity may be affected by the gut microbiota through energy harvesting and fat storage by the bacteria. Small intestinal bacterial overgrowth is also responsible for endotoxemia, systemic inflammation, and its consequences including obesity and nonalcoholic fatty liver disease (NAFLD). Relationship between gut microbiota and NAFLD is also dependent on altered choline and bile acid metabolism and endogenous alcohol production by gut bacteria. Further evidence linking gut microbiota with obesity and NAFLD comes from studies showing usefulness of probiotics in animals and patients with NAFLD. This article reviews the relationship among gut microbiota, obesity, and NAFLD.

http://www.ncbi.nlm....pubmed/24165893
Cell Res. 2014 Jan;24(1):5-6. doi: 10.1038/cr.2013.142. Epub 2013 Oct 29.
An antibiotic-altered microbiota provides fuel for the enteric foe.
Stiemsma LT1, Turvey SE2, Finlay BB1.
Author information
Abstract
Antibiotic therapies disrupt the intestinal microbiota and render the host susceptible to enteric infections. A recent report by Ng et al. explores the ability of two intestinal pathogens (Salmonella enterica serovar Typhimurium and Clostridium difficile) to use this disruption to their advantage and consume host carbohydrates that would otherwise be unavailable in the presence of a normal gut microbiota.

http://www.ncbi.nlm....pubmed/24123746
Appl Environ Microbiol. 2014 Jan;80(1):9-18. doi: 10.1128/AEM.02977-13. Epub 2013 Oct 11.
Genomic Overview and Biological Functions of Exopolysaccharide Biosynthesis in Bifidobacterium spp.
Hidalgo-Cantabrana C, Sánchez B, Milani C, Ventura M, Margolles A, Ruas-Madiedo P.
Author information
Abstract
For many years, bacterial exopolysaccharides (EPS) have received considerable scientific attention, mainly due to their contribution to biofilm formation and, above all, because EPS are potential virulence factors. In recent times, interest in EPS research has enjoyed a welcome boost thanks to the discovery of their ability to mediate communication processes with their surrounding environment and to their contribution to host health maintenance. In this review, we provide a fresh perspective on the genetics and activity of these polymers in members of the Bifidobacterium genus, a common gut inhabitant of humans and animals that has been associated with several health-promoting effects. Bifidobacteria can use EPS to protect themselves against the harsh conditions of the gastrointestinal tract, thus improving their persistence in the host. Indeed, the relevant function of EPS for bifidobacteria is underlined by the fact that most genomes sequenced until now contain genes related to EPS biosynthesis. A high interspecies variability in the number of genes and structural organization is denoted among species/subspecies; thus, eps clusters in this genus do not display a consensus genetic architecture. Their different G+C content compared to that of the whole genome suggests that eps genes have been acquired by horizontal transfer. From the host perspective, EPS-producing bifidobacteria are able to trigger both innate and adaptive immune responses, and they are able to modulate the composition and activity of the gut microbiota. Thus, these polymers seem to be critical in understanding the physiology of bifidobacteria and their interaction with the host.

http://www.ncbi.nlm....pubmed/24114492
Cancer Treat Res. 2014;159:377-99. doi: 10.1007/978-3-642-38007-5_22.
Gut microbes, diet, and cancer.
Hullar MA, Burnett-Hartman AN, Lampe JW.
Author information
Abstract
An expanding body of evidence supports a role for gut microbes in the etiology of cancer. Previously, the focus was on identifying individual bacterial species that directly initiate or promote gastrointestinal malignancies; however, the capacity of gut microbes to influence systemic inflammation and other downstream pathways suggests that the gut microbial community may also affect risk of cancer in tissues outside of the gastrointestinal tract. Functional contributions of the gut microbiota that may influence cancer susceptibility in the broad sense include (1) harvesting otherwise inaccessible nutrients and/or sources of energy from the diet (i.e., fermentation of dietary fibers and resistant starch); (2) metabolism of xenobiotics, both potentially beneficial or detrimental (i.e., dietary constituents, drugs, carcinogens, etc.); (3) renewal of gut epithelial cells and maintenance of mucosal integrity; and (4) affecting immune system development and activity. Understanding the complex and dynamic interplay between the gut microbiome, host immune system, and dietary exposures may help elucidate mechanisms for carcinogenesis and guide future cancer prevention and treatment strategies.

http://www.ncbi.nlm....pubmed/24399149
Mucosal Immunol. 2014 Jan 8. doi: 10.1038/mi.2013.117. [Epub ahead of print]
Fecal microbiota transplantation: effectiveness, complexities, and lingering concerns.
Pamer EG.
Author information
Abstract
The mammalian colon is home to a microbial ecosystem that enhances resistance to infection, stimulates mucosal immune defenses, synthesizes essential vitamins, and promotes caloric uptake by hydrolyzing complex carbohydrates. The bacterial populations inhabiting the gut are complex and vary between different individuals. Clinical and experimental studies reveal that the colonic microbiota can enhance or ameliorate intestinal and systemic inflammatory diseases. Because of its potential to enhance resistance to infection and to reduce inflammatory diseases, targeted manipulation of microbial populations is a growing focus of investigation. The most dramatic manipulation of the intestinal microbiota involves fecal microbiota transplantation (FMT) from healthy donors to individuals with specific diseases. Remarkable clinical effectiveness of FMT has been demonstrated for recurrent Clostridium difficile infection and ongoing studies are investigating FMT for other diseases. Transplantation of complex microbial populations to recipients likely triggers mucosal immune responses that, depending on the microbiota composition and the recipient's genotype, could range from pro- to anti-inflammatory. The impact of FMT on the recipient immune system is complex and unpredictable. Ongoing discovery of commensal microbes and investigations of their impact on the host will lead to the development of new probiotic agents and microbial consortia that will eventually replace FMT.Mucosal Immunology advance online publication, 8 January 2014. doi:10.1038/mi.2013.117.

http://www.ncbi.nlm....pubmed/24390924
Semin Reprod Med. 2014 Jan;32(1):74-86. doi: 10.1055/s-0033-1361825. Epub 2014 Jan 3.
Early development of the gut microbiome and immune-mediated childhood disorders.
Li M, Wang M, Donovan SM.
Author information
Abstract
The human gastrointestinal tract inhabits a complex microbial ecosystem that plays a vital role in host health through its contributions to nutrient synthesis and digestion, protection from pathogens, and promoting maturation of host innate and adapt immune systems. The development of gut microbiota primarily occurs during infancy and is influenced by multiple factors, including prenatal exposure; gestational age; mode of delivery; feeding type; pre-, pro-, and antibiotic use; and host genetics. In genetically susceptible individuals, changes in the gut microbiota induced by environmental factors may contribute to the development of immune-related disorders in childhood, including atopic diseases, inflammatory bowel disease, irritable bowel syndrome, and necrotizing enterocolitis. Pre- and probiotics may be useful in the prevention and treatment of some immune-related diseases by modulating gut microbiota and regulating host mucosal immune function. The review will discuss recent findings on the environmental factors that influence development of gut microbiota during infancy and its potential impact on some immune-related diseases in childhood. The use of pre- and probiotics for prevention and intervention of several important diseases in early life will also be reviewed.

http://www.ncbi.nlm....pubmed/24390923
Semin Reprod Med. 2014 Jan;32(1):68-73. doi: 10.1055/s-0033-1361824. Epub 2014 Jan 3.
A review of the source and function of microbiota in breast milk.
Latuga MS1, Stuebe A2, Seed PC3.
Author information
Abstract
Breast milk contains a rich microbiota composed of viable skin and non-skin bacteria. The extent of the breast milk microbiota diversity has been revealed through new culture-independent studies using microbial DNA signatures. However, the extent to which the breast milk microbiota are transferred from mother to infant and the function of these breast milk microbiota for the infant are only partially understood. Here, we appraise hypotheses regarding the formation of breast milk microbiota, including retrograde infant-to-mother transfer and enteromammary trafficking, and we review current knowledge of mechanisms determining the extent of breast milk microbiota transfer from mother to infant. We highlight known functions of constituents in the breast milk microbiota-to enhance immunity, liberate nutrients, synergize with breast milk oligosaccharides to enhance intestinal barrier function, and strengthen a functional gut-brain axis. We also consider the pathophysiology of maternal mastitis with respect to a dysbiosis or abnormal shift in the breast milk microbiota. In conclusion, through a complex, highly evolved process in the early stages of discovery, mothers transfer the breast milk microbiota to their infants to impact infant growth and development.

http://www.ncbi.nlm....pubmed/24388028
Mayo Clin Proc. 2014 Jan;89(1):107-14. doi: 10.1016/j.mayocp.2013.10.011.
A Clinician's Primer on the Role of the Microbiome in Human Health and Disease.
Khanna S1, Tosh PK2.
Author information
Abstract
The importance of the commensal microbiota that colonizes the skin, gut, and mucosal surfaces of the human body is being increasingly recognized through a rapidly expanding body of science studying the human microbiome. Although, at first glance, these discoveries may seem esoteric, the clinical implications of the microbiome in human health and disease are becoming clear. As such, it will soon be important for practicing clinicians to have an understanding of the basic concepts of the human microbiome and its relation to human health and disease. In this Concise Review, we provide a brief introduction to clinicians of the concepts underlying this burgeoning scientific field and briefly explore specific disease states for which the potential role of the human microbiome is becoming increasingly evident, including Clostridium difficile infection, inflammatory bowel disease, colonization with multidrug-resistant organisms, obesity, allergic diseases, autoimmune diseases, and neuropsychiatric illnesses, and we also discuss current and future roles of microbiome restorative therapies.

http://www.ncbi.nlm....pubmed/24328376
Future Microbiol. 2014 Jan;9:13-6. doi: 10.2217/fmb.13.141.
How enteric pathogens know they hit the sweet spot.
Alvarado I, Abel-Santos E.
Author information
Abstract
EVALUATION OF:
Ng KM, Ferreyra JA, Higginbottom SK et al. Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens. Nature 502(7469), 96-99 (2013). The human gut microbiota is a complex system of commensal microorganisms required for normal host physiology. Disruption of this protective barrier by antibiotics creates opportunities for enteric pathogens to establish infections. Although the correlation between the use of antibiotics and enteric infections have been known for some time, the specific signals that allow enteric pathogens to recognize a susceptible host have not been determined. In a recent article, Ng et al. demonstrated that the expansion of both Salmonella typhimurium and Clostridium difficile infections is enhanced by the availability of host-specific sugars liberated from the intestinal mucus by commensal bacteria. These results show how antibiotic removal of specific species from the gut microbiome allows symbiotic functions to be hijacked by pathogenic species.

http://www.ncbi.nlm....pubmed/24382146
Br J Nutr. 2014 Jan 2:1-6. [Epub ahead of print]
Dietary supplementation with lactose or artificial sweetener enhances swine gut Lactobacillus population abundance.
Daly K1, Darby AC1, Hall N1, Nau A2, Bravo D2, Shirazi-Beechey SP1.
Author information
Abstract
The commensal bacteria Lactobacillus are widely used as probiotic organisms conferring a heath benefit on the host. They have been implicated in promoting gut health via the stimulation of host immunity and anti-inflammatory responses, as well as protecting the intestinalmucosa against pathogen invasion. Lactobacilli grow by fermenting sugars and starches and produce lactic acid as their primary metabolic product. For efficient utilisation of varied carbohydrates, lactobacilli have evolved diverse sugar transport and metabolic systems, which are specifically induced by their own substrates. Many bacteria are also capable of sensing and responding to changes in their environment. These sensory responses are often independent of transport or metabolism and are mediated through membrane-spanning receptor proteins. We employed DNA-based pyrosequencing technology to investigate the changes in the intestinal microbiota of piglets weaned to a diet supplemented with either a natural sugar, lactose or an artificial sweetener (SUCRAM®, consisting of saccharin and neohesperidin dihydrochalcone (NHDC); Pancosma SA). The addition of either lactose or saccharin/NHDC to the piglets' feed dramatically increased the caecal population abundance of Lactobacillus, with concomitant increases in intraluminal lactic acid concentrations. This is the first report of the prebiotic-like effects of saccharin/NHDC, an artificial sweetener, being able to influence the commensal gut microbiota. The identification of the underlying mechanism(s) will assist in designing nutritional strategies for enhancing gut immunity and maintaining gut health.

http://www.ncbi.nlm....pubmed/24389673
Curr Opin Clin Nutr Metab Care. 2014 Jan 2. [Epub ahead of print]
Biological significance of short-chain fatty acid metabolism by the intestinal microbiome.
Puertollano E, Kolida S, Yaqoob P.
Author information
Abstract
PURPOSE OF REVIEW:
Evidence suggests that short-chain fatty acids (SCFAs) derived from microbial metabolism in the gut play a central role in host homeostasis. The present review describes the current understanding and physiological implications of SCFAs derived from microbial metabolism of nondigestible carbohydrates.
RECENT FINDINGS:
Recent studies indicate a role for SCFAs, in particular propionate and butyrate, in metabolic and inflammatory disorders such as obesity, diabetes and inflammatory bowel diseases, through the activation of specific G-protein-coupled receptors and modification of transcription factors. Established prebiotics, such as fructooligosaccharides and galactooligosaccharides, which support the growth of Bifidobacteria, mainly mediate acetate production. Thus, recent identification of prebiotics which are able to stimulate the production of propionate and butyrate by benign saccharolytic populations in the colon is of interest.
SUMMARY:
Manipulation of saccharolytic fermentation by prebiotic substrates is beginning to provide information on structure-function relationships relating to the production of SCFAs, which have multiple roles in host homeostasis.

http://www.ncbi.nlm....pubmed/24332541
Curr Biol. 2014 Jan 6;24(1):40-9. doi: 10.1016/j.cub.2013.10.077. Epub 2013 Dec 12.
An Ecological Network of Polysaccharide Utilization among Human Intestinal Symbionts.
Rakoff-Nahoum S1, Coyne MJ2, Comstock LE3.
Author information
Abstract
BACKGROUND:
The human intestine is colonized with trillions of microorganisms important to health and disease. There has been an intensive effort to catalog the species and genetic content of this microbial ecosystem. However, little is known of the ecological interactions between these microbes, a prerequisite to understanding the dynamics and stability of this host-associated microbial community. Here we perform a systematic investigation of public goods-based syntrophic interactions among the abundant human gut bacteria, the Bacteroidales.
RESULTS:
We find evidence for a rich interaction network based on the breakdown and use of polysaccharides. Species that utilize a particular polysaccharide (producers) liberate polysaccharide breakdown products (PBPs) that are consumed by other species unable to grow on the polysaccharide alone (recipients). Cross-species gene addition experiments demonstrate that recipients can grow on a polysaccharide if the producer-derived glycoside hydrolase, responsible for PBP generation, is provided. These producer-derived glycoside hydrolases are public goods transported extracellularly in outer membrane vesicles allowing for the creation of PBP and concomitant recipient growth spatially distant from the producer. Recipients can exploit these ecological interactions and conditionally outgrow producers. Finally, we show that these public goods-based interactions occur among Bacteroidales species coresident within a natural human intestinal community.
CONCLUSIONS:
This study examines public goods-based syntrophic interactions between bacterial members of the human gut microbial ecosystem. This polysaccharide-based network likely represents foundational relationships creating organized ecological units within the intestinal microbiota, knowledge of which can be applied to impact human health.

http://www.ncbi.nlm....pubmed/24355793
J Nutr Biochem. 2013 Oct 29. pii: S0955-2863(13)00210-6. doi: 10.1016/j.jnutbio.2013.09.009. [Epub ahead of print]
Influence of dietary fat on intestinal microbes, inflammation, barrier function and metabolic outcomes.
Shen W1, Gaskins HR2, McIntosh MK3.
Author information
Abstract
Recent studies using germ-free, gnotobiotic microbial transplantation/conventionalization or antibiotic treatment in rodent models have highlighted the critical role of intestinal microbes on gut health and metabolic functions of the host. Genetic and environmental factors influence the abundance and type of mutualistic vs. pathogenic bacteria, each of which has preferred substrates for growth and unique products of fermentation. Whereas some fermentation products or metabolites promote gut function and health, others impair gut function, leading to compromised nutrient digestion and barrier function that adversely impact the host. Such products may also influence food intake, energy harvest and expenditure, and insulin action, thereby influencing adiposity and related metabolic outcomes. Diet composition influences gut microbiota and subsequent fermentation products that impact the host, as demonstrated by prebiotic studies using oligosaccharides or other types of indigestible fiber. Recent studies also show that dietary lipids affect specific populations of gut microbes and their metabolic end products. This review will focus on studies examining the influence of dietary fat amount and type on the gut microbiome, intestinal health and positive and negative metabolic consequences. The protective role of omega-3-rich fatty acids on intestinal inflammation will also be examined.

http://www.ncbi.nlm....pubmed/24314205
J Appl Microbiol. 2013 Dec 7. doi: 10.1111/jam.12415. [Epub ahead of print]
Summer Meeting 2013: growth and physiology of bifidobacteria.
De Vuyst L, Moens F, Selak M, Rivière A, Leroy F.
Author information
Abstract
Bifidobacteria are a minor fraction of the human colon microbiota with interesting properties for carbohydrate degradation. Monosaccharides such as glucose and fructose are degraded through the bifid shunt, a dedicated pathway involving phosphoketolase activity. Its stoechiometry learns that three moles of acetate and two moles of lactate are produced per two moles of glucose or fructose that are degraded. However, deviations from this 3 : 2 ratio occur, depending on the rate of substrate consumption. Slower growth rates favour the production of acetate and pyruvate catabolites (such as formate) at the cost of lactate. Interestingly, bifidobacteria are capable to degrade inulin-type fructans (ITF) (oligofructose and inulin) and arabinoxylan-oligosaccharides (AXOS). Beta-fructofuranosidase activity enables bifidobacteria to degrade ITF. However, this property is strain-dependent. Some strains consume both fructose and oligofructose, with different preferences and degradation rates. Small oligosaccharides (degree of polymerization or DP of 2-7) are taken up, in a sequential order, indicating intracellular degradation and as such giving these bacteria a competitive advantage towards other inulin-type fructan degraders such as lactobacilli, bacteroides and roseburias. Other strains consume long fractions of oligofructose and inulin. Exceptionally, oligosaccharides with a DP of up to 20 (long-chain inulin) are consumed by specific strains. Also, the degradation of AXOS by α-arabinofuranosidase and β-xylosidase is strain-dependent. Particular strains consume the arabinose substituents, whether or not together with a consumption of the xylose backbones of AXOS, either up to xylotetraose or higher and either extra- or intracellularly. The production of high amounts of acetate that accompanies inulin-type fructan degradation by bifidobacteria cross-feeds other colon bacteria involved in the production of butyrate. However, bifidobacterial strain-dependent differences in prebiotic degradation indicate the existence of niche-specific adaptations and hence mechanisms to avoid competition among each other and to favour coexistence with other colon bacteria.

http://www.ncbi.nlm....les/PMC3705355/
Nutrients. 2013 Apr 22;5(4):1417-35. doi: 10.3390/nu5041417.
Fiber and prebiotics: mechanisms and health benefits.
Slavin J.
Author information
Abstract
The health benefits of dietary fiber have long been appreciated. Higher intakes of dietary fiber are linked to less cardiovascular disease and fiber plays a role in gut health, with many effective laxatives actually isolated fiber sources. Higher intakes of fiber are linked to lower body weights. Only polysaccharides were included in dietary fiber originally, but more recent definitions have included oligosaccharides as dietary fiber, not based on their chemical measurement as dietary fiber by the accepted total dietary fiber (TDF) method, but on their physiological effects. Inulin, fructo-oligosaccharides, and other oligosaccharides are included as fiber in food labels in the US. Additionally, oligosaccharides are the best known "prebiotics", "a selectively fermented ingredient that allows specific changes, both in the composition and/or activity in the gastrointestinal microflora that confers benefits upon host well-bring and health." To date, all known and suspected prebiotics are carbohydrate compounds, primarily oligosaccharides, known to resist digestion in the human small intestine and reach the colon where they are fermented by the gut microflora. Studies have provided evidence that inulin and oligofructose (OF), lactulose, and resistant starch (RS) meet all aspects of the definition, including the stimulation of Bifidobacterium, a beneficial bacterial genus. Other isolated carbohydrates and carbohydrate-containing foods, including galactooligosaccharides (GOS), transgalactooligosaccharides (TOS), polydextrose, wheat dextrin, acacia gum, psyllium, banana, whole grain wheat, and whole grain corn also have prebiotic effects.

Edited by lostfalco, 29 January 2014 - 03:51 PM.

[lostfalco]

Just to clarify...I'm recommending PREbiotics first. Prebiotics = food for good bacteria. Probiotics = good bacteria themselves. I think that most people already have the good bacteria, they just need to feed them (obviously, there will be exceptions). In most cases, probiotics are probably unnecessary. =)

I'll post abstracts to all of the 2014 studies that I'm currently going through in another post. Give me just one minute....

I'd recommend both instead. There is tons of research on individual strains (everything from making rats "glow" of health/beauty, curing Crohn's (well, that's mainly poop) to less bodyfat and better blood profiles), probiotic meals (kefir, sauerkraut, etc), all showing vert promising results. I'm guessing, due to the hygiene standards we have today, we've fucked up most of the bacterias we have. Introducing more ("good") strains when also adding prebiotics to help them, and the others, survive will most likely produce the best results.

Yeah, I think we totally agree here Nattzor. We may just differ a little on 'order of operations'. I'd simply say try prebiotics first and if that works, then no need to add probiotics. That's all. I think otherwise, we completely agree.

[hephaestus]

I just bought a bottle of this stuff from amazon:

http://www.amazon.co...0?ie=UTF8&psc=1

Started adding a tbsp of potato starch to my morning soylent.

http://quackfiles.bl...cs-warning.html

Looks like FUD spread by a manufacturer of a competing product to me.

I questioned numerous respected naturopaths, microbiology professors and gastroenterologists for their opinion on the product and all said it looked fine.

Then the founder and president of a company that sells a competing product comes along and she immediately changes her mind?

[Nattzor]

So, still in the planning stage of the helmet (I underestimated the planning needed). The only thing I've decided for atm is that I'm gonna use a construction helmet as the actual helmet.

Re wavelength: Is it worth mixing them, so I have some in the 600 nm range and some inte 800 nm range?

Would love if someone else was building one/planning on doing it would PM me and we could work on plans together.

[OpaqueMind]

The implications of those studies are staggering! Looks like there'll have to be a huge rethink of the foundations of health, both physical and mental. I find it ironic that the main thing which 'healthcare' providers do is dish out antibiotics, which in light of this evidence is pretty much the worst possible thing you could do for your health. Aside from snorting cyanide, obviously.

[middpanther88]

The studies are great and all, but has anyone actually tried the potato starch/prebiotics?

[BigPapaChakra]

Here's an alternative view on the whole RS http://digestiveheal...-friend-or-foe/

I've gotta do a ton of digging into this now. The idea of RS's benefits sound phenomenal to me, but then again there is the whole problem of persorption, endotoxin, and the fact that starch can be detected in CSF, blood, etc. which is, well... kind of frightening in its own right. Far too much information to develop firm stances on without tons of research, that's for sure.

[basicallyyes]

There are several supplemental O2 products such as Boost Oxygen that are readily available at Walmart. That being said there are many consumer reviews of these products. It seems under normal breathing conditions these people do not feel any significant nootropic effect but I saw a body builder review saying it helps replenish her when oxygen starved from continuous hard workouts so she can continue.

The nootropic effect of supplemental oxygen by itself seems insignificant to reviewers. But I would urge someone to try it in combination with the potent vasodilator properties of Vitamin B3 (niacin). I have read that some blood vessels in the brain are so small blood cells travel through in single file. To enhance the reach of the O2, perhaps combination with a vasodilator to deliver oxygen to oxygen starved parts of the brain may enhance the effects.

I've had good results with only O2. If you look at the studies, its primary nootropic effect is mostly evident during high mental exertion. Although, it does seem to help at other times as well.

With that said, the vasodilator idea is right on in my experience. I've combined O2 with a vibration plate...which makes me feel incredible. I've also used O2 with the laser (it's a vasodilator), vinpocetine, nicergoline, and combos of all of the above. Huge energy boost for hours.

I'm interested in this, do you remember specifically what combination gave you the best energy boost? Was it mental energy or did it feel like physical endurance?

[basicallyyes]

Hey guys ! just wanted to share with you the amazing change I'm experiencing with the LLLT.

I'm doing LLLT for around 3 month now- and the results keep amaze me. I didn't really realize how
Significant they actually were until today evening- as we had a social event and I meet a couple of guys
That I talk with a week ago.. and not only I remember all the names perfectly- but I recall exactly what this
person has told me, what he was specialized in and when he did it. As the conversations went on-
I felt unbelievable.My brain spit out every piece of information about this specific specialization with
the person with whom I talked to.. and it wasn't little. Soon people start to gather around.. I was kind of
afraid of that as I never use to be in the center of conversation- but I couldn't help it- the conversation
flow so smoothly as my brain connect the dots for me before I even realize that. And all the mentioned
has happened in a language that is not my native language, which makes it even more remarkable.

That being said- it took me some time to tune-up the LLLT routine, it's ongoing process . However, so far
the modification I did to the TULIP protocol are these :

[ all these ingredients were deeply researched beforehand. But more importantly, I've figure out the optimal dosage,
way of administration and optimal time of consumption according to the pharmacokinetics propeties of the substances. ]

[ only in days of LLLT ]
- 5g curcumine + 2g black pepper - both need to be dissolved in oil. preferably olive oil or fish oil
- 2g cinnamon - Need to be dissolved with a little hot water, and let sit for a while.
- 20 drops of diluted Methylene blue
- 10mg noopept
- 60mg Ginkgo Biloba ( pill )
- 200mg CoQ 10 ( pill )

All this need to be taken 1.5 - 2 hours before the LLLT treatment, as this is the peak concentration in the blood
of most of the mentioned agents.

All these agents are basically serve for their neuro-protective properties, that literally `buy some time` ,in order to prolong the time-per-spot

LED or Vetro?

[lostfalco]

The studies are great and all, but has anyone actually tried the potato starch/prebiotics?

Hey middpanther!

Yeah, hundreds of n=1's out there.

I originally found out about it from Joe Cohen http://selfhacked.co...-weight-loss
and Richard Nikoley's site has all the n=1's you could ever want. =) http://freetheanimal...er-newbies.html

Edited by lostfalco, 30 January 2014 - 03:50 PM.

[Raz007]

Hey guys ! just wanted to share with you the amazing change I'm experiencing with the LLLT.

I'm doing LLLT for around 3 month now- and the results keep amaze me. I didn't really realize how
Significant they actually were until today evening- as we had a social event and I meet a couple of guys
That I talk with a week ago.. and not only I remember all the names perfectly- but I recall exactly what this
person has told me, what he was specialized in and when he did it. As the conversations went on-
I felt unbelievable.My brain spit out every piece of information about this specific specialization with
the person with whom I talked to.. and it wasn't little. Soon people start to gather around.. I was kind of
afraid of that as I never use to be in the center of conversation- but I couldn't help it- the conversation
flow so smoothly as my brain connect the dots for me before I even realize that. And all the mentioned
has happened in a language that is not my native language, which makes it even more remarkable.

That being said- it took me some time to tune-up the LLLT routine, it's ongoing process . However, so far
the modification I did to the TULIP protocol are these :

[ all these ingredients were deeply researched beforehand. But more importantly, I've figure out the optimal dosage,
way of administration and optimal time of consumption according to the pharmacokinetics propeties of the substances. ]

[ only in days of LLLT ]
- 5g curcumine + 2g black pepper - both need to be dissolved in oil. preferably olive oil or fish oil
- 2g cinnamon - Need to be dissolved with a little hot water, and let sit for a while.
- 20 drops of diluted Methylene blue
- 10mg noopept
- 60mg Ginkgo Biloba ( pill )
- 200mg CoQ 10 ( pill )

All this need to be taken 1.5 - 2 hours before the LLLT treatment, as this is the peak concentration in the blood
of most of the mentioned agents.

All these agents are basically serve for their neuro-protective properties, that literally `buy some time` ,in order to prolong the time-per-spot

LED or Vetro?

Led, according to this protocol

Attached Files

•  pt.jpg   70.22KB   89 downloads

[Nattzor]

Found something really cool that I guess you might like.

http://www.plosone.o...al.pone.0039799 - "Pseudo-Synesthesia through Reading Books with Colored Letters"

[NeuroGeneration]

hey guys! been following this thread for months now, and have been LLLT / TULIP / tDCSing since October

Lostfalco - amazing job. You've really nurtured this thread to levels that only an LLLTer would be capable!

Re: prebiotics & probiotics. I've been using them for a while (began with making my own kefir & kombucha a few years ago), and have been taking unmodified potato starch & making green plantain chips in my oven. Both work very well, and are super cheap. You may want to take a look at this post, which focuses on the value behind inulin, and more importantly, GOS, as prebiotics. http://caloriesproper.com/?p=4153 Overall, I'd say that this blog has some kick-ass posts, from a super bright (and funny) PhD. I've ordered some GOS and am waiting for it to arrive from the UK.

Regarding the probiotics, if you're looking for the best, it seems that PrescriptAssist would currently hold that title. It has the most strains of soil-based probiotics, which have tremendous promise, and you may not be able to get from your standard diet (but evolutionarily speaking, we may have had from our less-than-hygenic eating practices!). A runner-up might be Bio-Kult. A nice thing about PrescriptAssist is after 30 days of 2 pills/day, you maintain with only 1 - 2 pills/wk. I love cost savings

I've also begun experimenting with the probiotics mentioned on Dave Asprey's Bulletproof Exec podcast interview of Shamanic researcher / Doc Alberto Villoldo. They can be found here: http://ascendedhealth.com/. I got the Active Detox Probiotic (along with the standard probiotic), and they warn that they can cause flu-like symptoms. Although I didn't get that, I do think that it may be "running me down" a bit.

I'm curious if anyone has any opinions on this, based on its ingredients, and whether it's something I should discontinue, or it's a good sign of detox (ingredients: Structured water, noni, mangosteen, extracts and bacteriocins of L. plantarum and multiple strains of other beneficial microflora. Humic & Fulvic acids, chelators and Shilajit. Trace marine phytominerals and ocean salts. http://www.ascendedhealth.com/probiotics/Probiotic_ActiveDetox.htm).

Cheers!

[xks201]

You could save 70 bucks a month and eat dirt from your backyard and reap more health benefits.

[macropsia]

Has anyone had any thoughts as to how the minimum dosing logic would apply to non-brain sites? I just took a break from brain-LLLT (I just changed some other things in my regimen and have considerably ramped up my allergy-shot dosage and wanted to have a clearer idea of what was doing what) and have started using the LEDs (830 nm, same one everyone else has) on my neck for blood-irradiation/possible systemic anti-inflammatory effects (on the back; avoiding the thyroid for now).
Should I slowly ramp up the total time if I add brain-lllt? or is the non-brain LLLT a 'separate thing'? A lot of the studies on non-brain sites seem to use much higher doses.... but then again, the brain-doses used in studies also seem higher, which may not be necessary.
I was figuring it wouldn't matter, but it seems the dosage to the blood would be much higher if using brain and non-brain LLLT.

[lostfalco]

Of course, this is in rats so we have to keep that in mind. However, the prebiotic GOS elevated BDNF, NMDA receptor subunits, and D-serine. That is a pretty killer combo for learning and memory. Previous prebiotic studies have shown elevations in butyrate, HDAC acetylation, serotonin, neuropeptides, vitamin K, better absorption of dietary vitamins/minerals, lower inflammation, enhanced immune system function, lower cancer risk, etc. I think you guys can see why I'm a little excited here. =)

http://www.ncbi.nlm....pubmed/24140431
Neurochem Int. 2013 Dec;63(8):756-64. doi: 10.1016/j.neuint.2013.10.006. Epub 2013 Oct 16.
Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine.
Savignac HM, Corona G, Mills H, Chen L, Spencer JP, Tzortzis G, Burnet PW.
Author information

Abstract
The influence of the gut microbiota on brain chemistry has been convincingly demonstrated in rodents. In the absence of gut bacteria, the central expression of brain derived neurotropic factor, (BDNF), and N-methyl-d-aspartate receptor (NMDAR) subunits are reduced, whereas, oral probiotics increase brain BDNF, and impart significant anxiolytic effects. We tested whether prebiotic compounds, which increase intrinsic enteric microbiota, also affected brain BDNF and NMDARs. In addition, we examined whether plasma from prebiotic treated rats released BDNF from human SH-SY5Y neuroblastoma cells, to provide an initial indication of mechanism of action. Rats were gavaged with fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS) or water for five weeks, prior to measurements of brain BDNF, NMDAR subunits and amino acids associated with glutamate neurotransmission (glutamate, glutamine, and serine and alanine enantiomers). Prebiotics increased hippocampal BDNF and NR1 subunit expression relative to controls. The intake of GOS also increased hippocampal NR2A subunits, and frontal cortex NR1 and d-serine. Prebiotics did not alter glutamate, glutamine, l-serine, l-alanine or d-alanine concentrations in the brain, though GOSfeeding raised plasma d-alanine. Elevated levels of plasma peptide YY (PYY) after GOS intake was observed. Plasma from GOS rats increased the release of BDNF from SH-SY5Y cells, but not in the presence of PYY antisera. The addition of synthetic PYY to SH-SY5Y cell cultures, also elevated BDNF secretion. We conclude that prebiotic-mediated proliferation of gut microbiota in rats, like probiotics, increases brain BDNF expression, possibly through the involvement of gut hormones. The effect of GOS on components of central NMDAR signalling was greater than FOS, and may reflect the proliferative potency of GOS on microbiota. Our data therefore, provide a sound basis to further investigate the utility of prebiotics in the maintenance of brain health and adjunctive treatment of neuropsychiatric disorders.

Edited by lostfalco, 01 February 2014 - 03:58 PM.

[OpaqueMind]

Since GOS is a prebiotic and so is resistant starch, can we safely assume that they share the same downstream effects? Or do different prebiotics promote the proliferation of different bacterial strains?

EDIT; I feel like this topic deserves it's own thread. It seems to me that the sheer mishmash of topics in this thread is a detriment to proper information gathering :(

Edited by OpaqueMind, 01 February 2014 - 08:05 PM.

[macropsia]

Just guessing, but I think that would depend primarily on the sugars comprising your starches and whether the bacteria need to produce their own exoenzymes in order to hydrolyze it, or whether some species piggy-back on others to be able to use starch... or whether enough human amylase is present everywhere in the gut to provide for the microbiome, which would be my assumption. Given the population density down there, I would suspect there's a fair bit of 'sharing'. Glucose is a pretty universal 'food', so I imagine it would be difficult to get much specificity once the starch is broken down, but availability to different species may change.

edit: I certainly second Opaque's suggestion. It's already impossible to find anything in this thread lol.

Edited by macropsia, 01 February 2014 - 08:14 PM.

[lostfalco]

EDIT; I feel like this topic deserves it's own thread. It seems to me that the sheer mishmash of topics in this thread is a detriment to proper information gathering :(

That's a great point Opaque. This microflora topic is huge and pretty revolutionary as you said. I've already started 5 threads...I guess one more won't hurt. ha

[lostfalco]

edit: I certainly second Opaque's suggestion. It's already impossible to find anything in this thread lol.

Yours and Opaque's wishes are my command. I'm shooting for the Longecity record for most threads started. =) http://www.longecity...in-enhancement/

[Joe Cohen]

LF, I published your collation of the studies. Thanks. http://selfhacked.co...iet-is-healthy/

I gave you credit at the end. Not sure how you want to be referenced.

Btw, have you experimented with kombucha?

Edited by Joe Cohen, 01 February 2014 - 10:05 PM.

[Joe Cohen]

Effect of honey on the growth of and acid production by human intestinal Bifidobacterium spp.: an in vitro comparison with commercial oligosaccharides and inulin.

"Five human intestinal Bifidobacterium spp., B. longum, B. adolescentis, B. breve, B. bifidum, and B. infantis, were cultured..... Honey enhanced the growth of the five cultures much like FOS, GOS, and inulin did. Honey, FOS, GOS, and inulin were especially effective (P < 0.05) in sustaining the growth of these cultures after 24 h of incubation as compared with the control treatment. Overall, the effects of honey on lactic and acetic acid production by intestinal Bifidobacterium spp. were similar to those of FOS, GOS, and inulin."
I've been selfhacking with honey for years to improve cognitive performance, with good effect. Fructose doesn't go well with a high fat diet in my experience. Honey is advantageous to FOS, GOS and inulin in that it ALSO has powerful antimicrobial properties that kill negative bacteria in the gut. MUST BE RAW.

I have some honey's that I like best in my toolkit, but you are welcome to try your own honeys

Edited by Joe Cohen, 02 February 2014 - 10:45 PM.

[lostfalco]

LF, I published your collation of the studies. Thanks. http://selfhacked.co...iet-is-healthy/

I gave you credit at the end. Not sure how you want to be referenced.

Btw, have you experimented with kombucha?

Thanks man!

I've looked into it but haven't tried it yet. Just being cautious since a handful of people have had serious problems with it. Def gonna try it soon though.

Effect of honey on the growth of and acid production by human intestinal Bifidobacterium spp.: an in vitro comparison with commercial oligosaccharides and inulin.

"Five human intestinal Bifidobacterium spp., B. longum, B. adolescentis, B. breve, B. bifidum, and B. infantis, were cultured..... Honey enhanced the growth of the five cultures much like FOS, GOS, and inulin did. Honey, FOS, GOS, and inulin were especially effective (P < 0.05) in sustaining the growth of these cultures after 24 h of incubation as compared with the control treatment. Overall, the effects of honey on lactic and acetic acid production by intestinal Bifidobacterium spp. were similar to those of FOS, GOS, and inulin."
I've been selfhacking with honey for years to improve cognitive performance, with good effect. Fructose doesn't go well with a high fat diet in my experience. Honey is advantageous to FOS, GOS and inulin in that it ALSO has powerful antimicrobial properties that kill negative bacteria in the gut. MUST BE RAW.

I have some honey's that I like best in my toolkit, but you are welcome to try your own honeys

Thanks for the heads up Joe! I know you're way ahead of the curve on this. Have you tried XOS?

[Joe Cohen]

LF, I published your collation of the studies. Thanks. http://selfhacked.co...iet-is-healthy/

I gave you credit at the end. Not sure how you want to be referenced.

Btw, have you experimented with kombucha?

Thanks man!

I've looked into it but haven't tried it yet. Just being cautious since a handful of people have had serious problems with it. Def gonna try it soon though.

Effect of honey on the growth of and acid production by human intestinal Bifidobacterium spp.: an in vitro comparison with commercial oligosaccharides and inulin.

"Five human intestinal Bifidobacterium spp., B. longum, B. adolescentis, B. breve, B. bifidum, and B. infantis, were cultured..... Honey enhanced the growth of the five cultures much like FOS, GOS, and inulin did. Honey, FOS, GOS, and inulin were especially effective (P < 0.05) in sustaining the growth of these cultures after 24 h of incubation as compared with the control treatment. Overall, the effects of honey on lactic and acetic acid production by intestinal Bifidobacterium spp. were similar to those of FOS, GOS, and inulin."
I've been selfhacking with honey for years to improve cognitive performance, with good effect. Fructose doesn't go well with a high fat diet in my experience. Honey is advantageous to FOS, GOS and inulin in that it ALSO has powerful antimicrobial properties that kill negative bacteria in the gut. MUST BE RAW.

I have some honey's that I like best in my toolkit, but you are welcome to try your own honeys

Thanks for the heads up Joe! I know you're way ahead of the curve on this. Have you tried XOS?

I have not. I've tried IMO, GOS, FOS and Inulin in the past. I've been consuming MOS daily for the past 6 years in the form of nutritional yeast. It's been apart of my toolkit and RS diet. I've also been consuming honey and other prebiotics for a long time. RS was the most recent and started a year ago when I was researching insulin resistance. IMO, it was the most powerful. Various supps that I take and have my toolkit have prebiotic effects.

Prebiotic/prebiotic effects: NAG, Astragalus, Garlic, Berberine, RS, Fiber, Honey, Buckwheat, Flax, Nutritional yeast (Beta glucans, MOS), Fenugreek, Quercetin, Fisetin,

The whole RS diet really is focused on gut, brain and physical health. But people also must know that after a certain point the benefits start to decline. A balanced diet shouldn't need extra FODMAPs.



MOS

Experiments with rats have indicated that D-mannoheptulose injections created an aversion to carbohydrates.^[6] Glucomannan supplementation reputedly promotes weight loss in overweight persons as a result of fiber-filling and reduced fat uptake.^[7] But although a high fat diet supplemented with mannan oligosaccharide in mice reduced food intake, there was no significant effect on body weight, total fat, or visceral fat.^[8]
In farmed animals, gut health has an additional dimension, as a healthy gut enables more efficient use of feed, called the feed conversion ratio. Over many decades antibiotic drugs have been added to the diet of farmed animals at non-therapeutic levels in the absence of disease, in order to enhance the feed conversion ratio, accelerate growth and protect the animal's health, therefore increasing profitability for producers. Today, however, there is a global push to reduce the use of medically important antibiotics as feed additives for farm animals, due to concerns about this practice promoting the emergence of antibiotic resistant micro-organisms. This trend has fueled interest in natural nutritional concepts. Based on a large body of research MOS has established itself as a one of the more important natural additives in farm animal production. The effect of MOS on animal performance was analysed in several meta-analyses (statistical analyses of final reports from trials that essentially contain the same experimental treatments) for poultry,^{[9][10][11][12]} pigs,^[13][14] and calves.^[15]These analyses reported improvements in performance with MOS.
Effects of MOS on the intestinal microflora[edit]

As mentioned earlier MOS affects bacterial attachment in the intestinal tract. In controlled studies with chickens, a reduction in the prevalence and concentration of different strains of salmonella, as well as E. coli, was reported.^[16] Reductions in E. coli were also reported by several other researchers.^[17] Salmonella is a zoonoses, therefore an efficient control system, which includes dietary measures is critical in order to produce safe food. Further research has shown a reduction in clostridia, another common intestinal pathogen.^[18][19] The effects of MOS at controlling E. coli and salmonella are quite consistent. However, reported effects on promoting beneficial bacteria, such as lactobacilli and bifidobacteria are more variable.^[16][19][20] The application of molecular techniques allows us to study the composition of the intestinal microflora, giving us a more detailed picture of the complex changes following MOS supplementation.^[21][22]
Effects of MOS on intestinal structure and function[edit]

A large surface area is key for optimal digestive function, therefore the surface of the small intestine should be covered with long healthy villi. Yang et al.^[23] reported better energy digestion when including MOS in broilers. Several studies with MOS in poultry have looked at the intestinal structure and discovered longer villi and a more shallow crypt.^[24][25][26] Comparable changes in intestinal structure have also been reported in fish. In rainbow trout, supplementing the diet with 0.2% level of MOS resulted in an increase in gut surface area, microvilli length and density, and altered microbial populations.^[27]
A shallow crypt is a good indicator for an efficient small intestine, which requires fewer nutrients for renewal. With a low renewal rate the intestinal cells become more mature, allowing for more efficient digestive enzyme production and nutrient absorption. Research has shown increased production of enzymes such as; maltase, leucine aminopeptidase, and alkaline phosphatase with MOS.^[23][28]
To protect the villi and intestinal surface, the gut produces protecting mucus. This mucus is produced in specific cells called goblet cells. In general the number of goblet cells is an indicator of mucus production. Researchers found that goblet cell numbers were increased with MOS.^[20][24] The importance of those changes for animal health is still being debated by scientists.
MOS as a nutritional supplement for companion animals[edit]

MOS is included in diets for horses, dogs, cats, rabbits and birds by feed manufacturers, mainly due to its benefits for their health. MOS as a nutritional supplement offers a natural approach to support the microflora and thus improve overall health, well-being and longevity.
MOS for dogs[edit]

Rapid changes in the microflora and/or the proliferation of intestinal pathogens can lead to gastrointestinal diseases. Therefore, a number of trials have been carried out to explore the efficacy of MOS in improving gut health in dogs.
To reduce the risk of digestive upsets it is critical to keep the concentrations of potential pathogens low. MOS has been shown to reduce faecal E. coli and C. perfringens and tended to have greater concentrations of lactobacilli and bifidobacteria.^{[29][30][31][32]} Older dogs tend to have reduced concentrations of bifidobacteria.^[32] A significant increase in bifidobacteria concentration was noted with MOS supplementation to diets of senior dogs, thus counteracting the negative effect of age on colonic health.^[32]
The mechanism of action for reducing the numbers of C. perfringens may differ from that previously explained for bacteria with type-1-fimbriae. Research in other species has demonstrated that MOS has an effect on intestinal morphology as well as both innate and acquired immune system components, which may help to explain the observed reductions in C. perfringens. Research shows an increase in serum lymphocytes and lower plasma neutrophils when adult dogs were supplemented with MOS and FOS. These findings indicate an improvement in immunity that, in turn, gives rise to increased protection against intestinal pathogens.^[33]
Other areas of interest to dog owners are the effect of MOS on nutrient digestibility and stool quality; both for health and practical (poop-a-scoop) reasons.^[34][35]
MOS as a nutritional supplement for farm animals[edit]

Mannan oligosaccharides have been widely evaluated in feeding trials. As animal health and performance are influenced by many factors other than nutrition, the responses to a feed additive will vary between production systems. Therefore, a concept such as MOS should not be evaluated based on single trials. A meta-analyses, which summarizes a large number of published research trials allows for a more comprehensive overview.
MOS for poultry[edit]

The first study testing MOS in poultry showing an improvement in performance was peer-reviewed published in 2001.^[25] It showed an improvement in feed conversion, indicating that birds are converting feed more efficiently into body tissue. An efficient feed conversion ratio (FCR) is important for the overall efficiency and thus is a key contributing factor to sustainable poultry production. In addition, it is of great economic importance to the producer. Over the years, a series of papers looking at performance effects under different production conditions were published. Hooge ^[9]summarized 44 comparisons in a meta-analyses where MOS was fed between 0.5 to 2 kg / tonne of feed. He concluded that on average MOS led to 1.6% improvements in body weight, 2.0% improvement in FCR and lower bird mortality. Prof. Dr. Gordon Rosen,^[10] in his review of 82 comparisons, reported similar effects. After broilers (meat-producing chicken), turkey is the second most important source of poultry meat globally. In turkeys 76 comparisons have shown similar responses to MOS as in broilers.^[11][12] Several studies also suggest that MOS, when added to poultry diets, allows the birds to perform at a similar level as when fed a diet supplemented with antibiotic growth promoters (AGPs).^[19][36][37]
MOS for pigs[edit]

Part of a successful start into a piglet's life is the consumption of sufficient colostrum (milk from the sow the first day after birth). Colostrum contains high levels of immunoglobulins, which protect the piglet from harmful diseases in the first weeks of its life. Several studies have looked at supplementing sow diets with MOS with the aim of improving the health of the sows. A healthy sow produces good quality colostrum and spreads less harmful bacteria in the environment where she gives birth and raises the piglets. Several researchers have reported a significant increase in colostrum production ^[38] and colostrum quality ^[38] with MOS. Those changes in colostrum quality and quantity likely explain a reduced pre-weaning mortality and a higher litter size and litter weight at weaning ^[38] and can thereby help to better protect the piglet from disease, thus improving piglet survival. A recent review of published literature showed that the mortality of young piglets was reduced when MOS was supplemented in the diets of the sow.^[38] Keeping the mortality of young piglets to a minimum is important from an economical as well as from an animal welfare point of view.
The next critical phase in a piglet’s life is the time of weaning, when it is separated from the sow. The change from milk to solid feed leads to changes in the intestinal microflora and structure and thus presents a higher risk of intestinal problems. Two meta-analyses involving a total of 123 comparison,^[13][14] concluded that performance was better in piglets fed MOS-supplemented feed. The data also indicated that piglets, which were particularly challenged during this transition phase (showing a slower growth rate due to the challenge), responded particularly well to MOS supplements. Positive performance effects with MOS were also reported in later production phases, however, those effects appear to be smaller than in the very young animals.^[14]
MOS for calves[edit]

The first trial ever reported with MOS was with young bull calves.^[5] Newman et al.^[5] noted improved intake and subsequently better growth rates. The health status of young calves is one of the most important factors contributing to growth and performance. Diarrhoea in young calves is a major issue in the dairy sector. The cause can be viral or bacterial, however, E.coli is often involved. As MOS can bind E. coli (see Effects of MOS on the intestinal microflora), it can modify and help to improve the composition of the intestinal microflora. This resulted in a reduction in faecal E. coli counts^[17] and improvements in faecal score^[39] in calves fed MOS. These improvements were coupled with an increase in concentrate (dry feed) intake^[40] and better performance.^{[5][40][41][42][43]} In addition to the changes in the gut, several authors also noticed improvements in respiratory health, which can also contribute to better performance.^[5][41]Conversely, one trial reported no effects on liveweight gain despite increased feed intake.^[44] Higher liveweight gain, similar to that gained with the use of antibiotics, has been achieved following supplementation of milk replacer with MOS.^[45]
Dairy cows fed MOS had better immune protection against rotavirus and were able to pass some of this protection on to their calves.^[46] The transfer of immunity from the cow to the calves is critical in order to protect the calf from many different diseases.^[45]
MOS for aquaculture[edit]

Farmed Fish larvae are often fed with live feed cultures. As the intensive nature of live feed cultures provide ideal conditions for the growth of opportunistic pathogens, MOS incorporation into live feeds has been studied to assess the impact on the microbial load, particularly with regards to Vibrio species levels. MOS showed a reduction in Vibrio levels of live feed cultures.^[47][48][49] These reductions were likely due to the agglutination or binding of Vibrio cells to MOS mediated by the presence of mannose receptors. MOS supplementation has also been shown to reduce the overall cultivable intestinal microbial load ^[27] and to enhance species richness.^[50]
Several researchers have reported improved performance and feed efficiency with MOS in aqua culture.^[51][52] As in terrestrial animals, changes have been associated with effects on the gut and the immune system. Dimitroglou et al.^[50] observed alterations of circulating leukocytes proportions as well as increased total leucocyte levels when feeding gilthead sea bream. Torrecillas et al.^[53][54][55] assessed the dietary inclusion of various levels of MOS on the immune status and disease resistance of sea bass. MOS reduced Vibrio alginolyticus, Vibrio anguillarum andListonella anguillarum, two important pathogens in aqua fish.
Structure defines function[edit]

In the yeast cell wall, mannan oligosaccharides are present in complex molecules that are linked to the protein moiety. There are two main locations of mannan oligosaccharides in the surface area of Saccharomyces cerevisiae cell wall.^[56] They can be attached to the cell wall proteins^[57] as part of –O and –N glycosyl groups and also constitute elements of large α-D-mannanose polysaccharides^[58] (α-D-Mannans), which are built of α-(1,2)- and α-(1,3)- D-mannose branches (from 1 to 5 rings long), which are attached to long α-(1,6)-D-mannose chains.^[59] This specific combination of various functionalities involves mannan oligosacharides-protein conjugates and highly hydrophilic and structurally variable 'brush-like' mannan oligosaccharides structures that can fit to various receptors of animal digestive tracts,^[60] and to the receptors on the surface of bacterial membranes,^[61] impacts these molecules bioactivity. Mannan oligosacharides-protein conjugates are involved in interactions with the animal's immune system and as result enhance immune system activity.^[62] They also play a role in animal antioxidant and antimutagenicdefense.^[63]

Edited by Joe Cohen, 02 February 2014 - 11:56 PM.

[cylack]

So I looked up sources of GOS besides the expensive supplements sold. There is a Japanese yogurt called Yakult sold that has it, but its not widely available in the US. Interestingly, baby foods have GOS added. Don't know how much though, but GOS is listed as one of the first ingredients on baby food such as Similac. From Similac's website: Similac baby formulas are designed to be more like breast milk and help support your baby's developing immune system. And Similac baby formulas with EarlyShield have immune-supporting nucleotides — and prebiotics and carotenoids, nutrients naturally found in breast milk. In addition to having DHA/ARA, Similac has Lutein, an important nutrient babies can get from breast milk and Similac. It's especially helpful now, during this critical time of your baby's brain and eye development.

This is sorta crazy to think about taking this, but since this stuff is supposed to mimic mother's milk, would it be healthy for an adult to consume? I'm reluctant to try it because it has things I don't want to consume like manganese and iron. Anyone know how this stuff tastes?

Right now i'm taking about 2 tablespoons of resistant potato starch with a little bit of kefir and honey. I try to eat asparagus a couple times a week. Would like to add GOS to the diet just for some more diversity.

[alpal]

I'm considering starting on Resistant Starch such as http://www.amazon.co.../dp/B0013JOKBC/

I want to increase BDNF

What I'd like to know:

Has anyone experience significantly better focus/working memory/cognition from using prebiotics?

Should I be using a different prebiotic better suited for BDNF production?

Dosages?

I would really appreciate these answers! I'll be sure to record my results!

[basicallyyes]

Hey guys I just found out I have a stomach ulcer and thought about using a laser to heal it based on what I've read here and also :

http://health.usnews...ulcer/treatment
Laser: A laser light can be focused on a bleeding point to induce rapid tissue heating, which leads to coagulation. Clinical trials of ulcer hemorrhage have confirmed that photocoagulation with a laser effectively seals bleeding and nonbleeding visible vessels at risk of future hemorrhage. Important considerations that limit emergency laser treatment include portability of the lasers and cost; the need for specific expertise by the endoscopist and technician as well as special electrical outlets and eye protection; and technical considerations such as the difficulty in aiming the laser beam..

From what I've read and understand I would need a laser that is strong enough to penetrate deep enough - is the penetration dependent on the power? I was looking purchasing this:


http://shop.vetrolas...er-76565443.htm

but it is only 5mw - do you think that's strong enough to go about four-five inches?

I also have this I could try posted by falco:

http://www.ebay.com/...=item3cbaee2b2b

Edited by basicallyyes, 03 February 2014 - 06:58 PM.