since the core is simply this synergy, the structures can be quite dynamic inhering in the host biochemistry and not overt
during biofilm formation individual bacteria pump out proteins that self-assemble outside the cell ‑ creating tangled networks of fibers that essentially glue the cells together into communities that keep the bacteria safer than they would be on their own
biofilms, besides being self-assembled from bacteria products, also self-heal
if they get damaged, they grow right back because they are living tissues ”
the earliest form of life was a microbial biofilm
the furry feeling on teeth is a biofilm polysaccaride matrix.
so you can see how the need to reduce sugar in the diet spans a continuum of complete elimination of all carbs to specific carbohydrate exclusion.
biofilms can use simple sugars in their construction quite well, and may, by anchoring themselves to the gut walls, be able to inhibit the bodies absorbtion of simple sugars and cherry pick them for themselves which is why scd takes so long to get results and is unstable in effect.
you can test for biofilm with enzyme formulations like no fenol/candex which attacks only the sugar houses, if you have a bad reaction to a capsule you have biofilm.
be cautious with this test if you have heart or other health issues as the toxic load released can be stunning. activated charcoal may help.
you may find it necessary to start with very small amounts like say 1/8th or in extreme instances 1/60th of a capsule and work up.
in severe cases of biofilm ingress in the gut, candex and the houstonni enzymes may initally be too strong and the enzymedica 'lacto' in small divided amounts and working up may be a gentler way to start
north american herb and spice oreganol, as a broad spectrum anti-viral/anti-fungal/anti-bacterial can help too, and in fact the spices used in cooking are all about biofilm control!
biofilm can be that intelligent that it releases chemicals to make the brain crave the foods that feed the bad biofilm best (i find grape and ver juice bad for this)
benign bacteria can change brain function away from constant anxiety, trauma and depression !
the microbiome produces proteins to influence how full the brain perceives us to be !
body acidity problems are a classic sign of bad biofilm/microbiome overgrowth
years ago i had a stomach virus and thinking it was heartburn, i took an alkalinser
it just about killed me
the partly sensible doctor i saw recommended neat, freshly squeezed lemon juice which i got from lemons in the garden and that worked
bad biofilm secretes acid but likes alkaline conditions
obviously the kidneys being a liquid to tissue interface are another prime target for biofilm, bedwetting will be a symptom of biofilm in the kidneys
bacterial vaginosis is a biofilm, it must have stealth since it's non inflammatory
biofilms comprise bacteria, yeast and viruses, but can also include protozoa, metazoa and arcahea, hence parasites can compound the issues
if you look at the enlarged version of the picture on the right you can see how the bacteria can build little caps to protect itself
no wonder cholera is such a bastard, the immune system can only ever get a portion of it
chronic viral infection/exposure to viral carriers suppresses the white blood cell production which fights pathogen infections therefore allowing biofilm to run amok turning off T-Bet in the intestinal wall . . . . . . . colitis, crohn's, ibs is the consequence
current research indicates that colitis and ibs are due to biofilm with high virulence factors, particularly in bacteria genes
the seminal vesicles are a significant repository of malign microbiome !
“ these tubular glands produce seminal fluid, are located in an environment that is temperature controlled and is rich in carbohydrates needed to feed bacteria ”
a limited course of colloidal silver, being particularly toxic to bacteria and broad spectrum in action can be a big help or in some cases essential to break a vicious cycle of virulent biofilm and inflammation
however this study says that nanoparticle silver may cause stem cell death so caution is needed
research is beginning on the viral side, obviously just as much is happening with viruses as bacteria and fungi in the gut, but viruses are very difficult to detect !
the biofilm that develops is a question of control by the immune system so any developmental issues or skewness of immune function explodes into malign biofilm which is what you see on the health boards of course
the other side is the guts ability to selectively supply growth factors to bacteria it perceives as friendly
babies imprint their immune system to modulate biofilm and this can go wrong in a lot of ways, for instance being bottle fed and not breast fed in the early months
too early vaccines of course as well
biofilm bacteria can release a poison that kills attackers, wether bacterial predators like amoeba, or phagocytic human immune cells study
these poisons are also going to have systemic effects on the host allowing opportunities for synergies with viruses and yeast and general depreciation of host function and immune defense response
this is a really good explanation for intractable intestinal conditions like colitis and chrons
steriods are only going to reduce the inflamation and will not be long term effective because the bacteria and biofilm are still there
biofilms are like human communities, they can produce stuff in a community that individuals cannot alone, divisions of labour and smarter than average bacteria providing templates for unique materials
it also explains why antibiotics can be so effective as they poison the bacteria directly, though biofilm bacteria have other defenses against antibiotics like the restriction of flow through the structures of the biofilm
an interesting synergy occured recently with myself, eileen and her daughter with a virus going around tasmania that really let the weakest spot for a bacterial infection get away, with eileen it was a cut in the head getting infected and blowing up a lymph node behind a breast, her daughter had swollen neck glands, and with me with it was a mild attack of appendicitis (not to be forgotten!)
an appendicitis attack is strongly characteristic because the pain comes in waves of increasing strength and hopefully peaks and the waves die off in strength
also the inital location of the pain is not on the appendix, but is what is called "referred", that is, near the belly button and moves closer to the appendix as the waves increase in strength
you also get a feeling like the pain would be relieved if you could shit, but generally, you can't
bcd and scd, because they make for more solid stools and in combination with enzymes, longer transit times, do have a tendency to make for a greater likelyhood of the appendix not being able to empty so well (working properly the appendix acts a probiotic scource for the colon)
kneeling chairs are better for reducing this effect as sitting for long periods in ordinary chairs scrunch the appendix and prostrate up, making for problems
if you have IBS, colitis, chrons or heart and circulation issues you really need to eliminate viral exposure to the extent possible, you are not going to recover with anything but minimal viral exposure
cystic fybrosis is a biofilm, with the biofilm bacteria producing a protein similar to one of the active ingredients in rattlesnake venom study
strep is a biofilm
ankylosing spondylitis is a biofilm condition
allergies can be caused by biofilm toxins pubmed
staph infections are fair dink biofilm so you really have blast your way into the infection by some sort of debridement, mechanical or chemically
the life research 'bacteria buster' (usa only?) appears to be effective against staph
bacteria buster is 'extracts of comfrey leaves and stems, ascorbic acid and isolates of extracts of comfrey leaves and stems' as a tincture
Janet writes of using it for a staph infection for her son around the ankle
“ I saturated cotton balls with the stuff and used bandaids to hold them directly on the sores. Within 20 minutes or so, all of the bandaids except one had fallen off, but since it was so close to Cody's bedtime and he complained it burned, I thought to try again the next day. Amazingly, he woke up the next morning and all of the green was gone, the raw patches had really shrunk and looked much better. I applied another dose mid morning and yet another at bedtime. The sores dramatically reduced down to where right now he only has two places where they were that are whitish tinged - I guess where the new skin is growing back so rapidly or maybe scar tissue?? ”
oreganol, 35% hydrogen peroxide, colloidal silver are also useful
when the staph bacteria get stressed they go to spore form which is very hard to kill so you have to watch for re-occurance
mrsa or not, it can be extrodinarily persistent with suppressed immune systems
it's extremely contagious, putting spores in the air
thin skin on the legs is a typical staph spot
don't let them do a punch biopsy, it can push the infection into the blood
infections are assisted by the viral exposure
cotton swabbing of an open wound speeds healing, imo it physically abrades biofilm and that's how it works study
“ painless and gentle probing of a wound with a dry cotton swab after surgery dramatically reduced infections in post-operative incision sites ”
biofilm can supress the T BET protein in dentric cells that down-regulates the cytokine tnf (tumour necrosis factor) alpha leading to inflamation and holes in the epithelial lining from epithelial cell death
the genes for this in the biofilm are contagious through fecal-oral and skin to skin contact, per say uc and presumably crohn's are contagious
wendy garrett and laurie glimcher on T-Bet
you can actually see where the researchers are not quite putting two and two together because they lack the biofilm/bcd perspective
they don't understand the active role of biofilm in silencing T-Bet which will have a viral component getting through to the dentric cells
don't forget their mouse model also had the regulatory t cells deleted, “all the adaptive immune system” in wendy's words
“ Ulcerative colitis and a related disorder, Crohn's disease, are known collectively as inflammatory bowel disease. Crohn's disease tends to involve the small intestine as well as the colon. Ulcerative colitis usually appears between ages 15 and 30 but also can begin in the 50s and 60s, especially in men. The disease is somewhat more common among men than women, whites than non-whites, and Ashkenazi Jewish individuals than non-Jewish individuals. ”
interesting research abstract
Biofilm formation in E. faecalis is presumed to play an important role in a number of enterococcal infections. We have previously identified a genetic locus provisionally named bop that is involved in maltose metabolism and biofilm formation. A transposon insertion into the second gene of the locus (bopB) resulted in loss of biofilm formation, while the non-polar deletion of this gene, together with parts of the flanking genes (bopA and bopC ) resulted in increased biofilm formation. A polar effect of the transposon insertion on a transcriptional regulator (bopD) was responsible for the reduced biofilm formation of the transposon mutant.
The amount of biofilm formed is related to the presence of maltose or glucose in the growth medium. While the wild-type strain was able to produce biofilm in medium containing either glucose or maltose, two mutants of this locus showed opposite effects. When grown in medium containing 1% glucose, the transposon mutant showed reduced biofilm formation (9%), while the deletion mutant produced more biofilm (110%) than the wild-type. When grown in medium containing 1% maltose, the transposon mutant was able to produce more biofilm than the wild-type strain (111%), while the deletion mutant did not produce biofilm (4%). Biofilm formation was not affected by the presence of several other sugar sources. In a gastrointestinal colonization model, the biofilm-negative mutant was delayed in colonization of the mouse intestinal tract.
The biofilm-positive phenotype of the wild-type strain seems to be associated with colonization of enterococci in the gut and the presence of oligosaccharides in food may influence biofilm formation and therefore colonization of enterococci in the gastrointestinal system.
full copy pdf
i was doubtful about biofilms being able to be formed on mobile, shedding surfaces like the gut but thinking about it white on the tongue is a biofilm on such a surface so obviously it can happen
what is interesting that this paper shows is the way bacteria can be mutated to give different reponses and this is a core idea that bacteria, viruses and yeast exchange genes to rapidly mutate to suit the enviroment and nutrition
it is interesting that they did just as well on simple sugars as complex which is what you would expect, its only the rapid absorption of simple sugars by the gut that keep them from using it (if absorption is impaired, then obviously more than a dietary approach is needed), but actually it does point to the need for a more sophisticated approach than the btvc permits, theres lots of implication with ingesting simple sugars as well, as can be seen with fruit juices like grape juices and their biofilm spore and live organism loading as well as a lot of simple sugars very liked by biofilms
this is actually a major insufficiency of the BTVC
because biofilms need a surface to anchor to, any gut biofilm must very invasively hooked into gut wall cells and enzyme proteases would probably give a nasty reaction, so probably its best to start with the houstonni hn-zyme first rather than pep.
a bad reaction to proteases may be indicative of invasively anchored biofilms on the intestine or stomach wall
the fur on teeth are a biofilm; bacteria, yeast and viruses in a polysaccaride matrix that they have constructed to facilitate their survival and growth
colitis is likely an invasive intestinal biofilm infection with virulent genes and a maladaptive immune response
evidence increasingly suggests that there is an association between the microbiota in the gut - bacteria, fungi and viruses - and the development of autoimmune disorders e.g. uveitis !
and humans are the symbiont
partner and host
in the stomach and
and difficult relationship
i think the key is understanding biofilm as intelligent
its a fundamental change in the way humans are viewed
we are just biofilm hosts
the gut can only absorb simple sugars
complex the chains
the more difficult it is for our own enzymes to cut them down and the biofilm
especially bacteria get in on the act
the biofilm in metabolising carbohydrates generates a lot of toxins which cause most of the problems, but they also interfere with the gut wall and function and immune system and can spread all through the body
they also create a lot of short chain fatty acids which end up in the liver
that obesity is a condition of micronutrient malnutrition (chromium!) in combination with less digestible starches is a useful way of looking at things, the huge significance of less digestible starches is not the loss in available energy to the consumer, but the way this energy feeds malign stomach flora (BIOFILM!) instead, inducting all sorts of inflammatory and metabolic dysfunction problems !
less digestible starches in grains greatly promote shelf life and pest resistance so since the beginning of the agricultural revolution there has been a growing imbalance (massively accelerating in recent years) between what suits the growers and their infrastructure financially and what suits the consumers nutritionally and healthwise!
obesity, tho symptomatic of biofilm also involves mineral and other nutritional deficiencies and a lack of the right sun and of course a thyroid stymied by biofilm toxins
pest resistance in wheat and other grains involves making the sugars more tightly linked and thus less accessible to pests , but also harder to digest for us and thus more available to biofilm
basically modern breeding has moved grains into the nutritionally negative zone and they are no longer a viable food !
things have been going backwards for hundreds of years since the agricultural revolution when growing grains got divorced from eating and farmers eating their own wheat and taking digestibilty into account in the varieties they planted
these issues massively accelerated after WW2
sugar is the preferred source of energy for biofilm and humans, who gets it first determines the problem level compounded of course by immune system dysregulation
so in a way it doesn't matter wether its table sugar or complex carbohydrates, its wether the biofilm is getting it first and is not being tamped back by the immune system
a new concept - estrobolome
basically gut bacteria that release enzymes that can digest estrogen !
a lot of autistic spectrum women seem to have lower estrogen levels or lose sufficient levels early in life and this may be due a malign biofilm with unbalanced preponderance of estrogen digesting bacteria
rather fascinating !
re: the 2008 summer drought in new zealand
DairyNZ principal scientist John Roche said inappropriate feeding of tapioca and molasses had led to a condition called acidosis in cows, resulting in poisoning and death.
When too much starch or sugar was rapidly introduced into a cow's diet it produced dangerous levels of lactic acid which could result in death, Dr Roche said.
"Although not ideal from a nutritional perspective, this is not an issue with feeds like palm kernel meal because of the low starch or sugar content.
"However, with feeds like tapioca, cereal, grains or molasses it is a recipe for disaster and the disaster is even greater when cows are hungry," he said.
they feed a bit of silage in tasmania in droughts to provide some of the right bacteria to keep the cattle going on the dry grass
practically, the cattle really pick up on the silage
nz herald article
"Stinky" also happens in humans especially autistic children or adults with systemic 'candida', the candida is in fact a biofilm
the condition arises from an impaired digestion permitting the overgrowth of a fermenting biofilm with various fermentation byproducts including various organic volatiles
" One compound (1-penten-3-ol) that was found in higher amounts in stinky whale tissues by the U.S. laboratory is known to occur during lipid oxidation of plant materials " study
the above is the sort of compound one might expect
from there it gets more complex as the toxins also impair liver function and indeed have many more systemic effects
in addition you get arsenic and mercury accumulation in marine mammals which has many humans parallels with various heavy metal toxicities including mercury from amalgams
this view of biofilm overgrowth is not popular with the medical community, but has been around for many years in the form of the 'specific carbohydrate diet' and now the 'biofilm carbohydrate diet', the approach and theory is quite different from the atkens diet
seaweed is composed of complex polysaccarides that are not very digestible to mammal atic digestive juices, but are accessible to biofilm enzyme systems hence feed the biofilm preferentially to absorbtion by the animal gut itself
i.e. the grey whale is being forced to a ruminant diet without the digestive apparatus for it, a bit of slowly fermenting cod thrown in would provide proteins for the biofilm
"For several decades, hunters and communities in Russia have also noted an odor that is similar to that observed in stinky gray whales in the meat of ringed seals, bearded seals, walruses, and the eggs of Murres. More recently fishers have noticed a similar odor in some cod" study
the establishment of malign biofilm is to be expected with any number of causative condtions, possibly viruses, bacteria and new bacteria mutations, cumulative organic toxins, starvation forcing diets different from what the evolutionary design of the digestive system is adapted for, new pathogenicity in a parasite etc.
i don't think the marine world is any different from the land phylogenera and health failure through malign biofilm overgrowth is a universal mechanism
marine mammals and birds have the disadvantage of bioaccumuation of various heavy metals, especially mercury from the seafood diet, which may have the potential to become unsequestered from their selenium granules and wreak havoc, that is, you can have a positive feedback loop locking down the inability of the host to deal with biofilm
news article may 2008
the siberian grey whales have got so stinky that their meat has become inedible for aboriginal whalers who feed off the meat - not even their dogs will eat it.
brave diners who have tried the meat suffered from numb mouths, stomach ache and skin rashes.
and seals, walruses and seabird eggs are giving off a similar smell according to locals.
usually the whales have a diet of shrimp like crustaceans called amphipods they filter from the sea bottom with their shortened baleen but hunters have found seaweed and cod in the stomach of the smelly whales.
the whales migrate from shores off the north of mexico to alaska but scientists believe that some whales are not making the journey all the way north and that amphipods are not found in their new feeding areas.
another theory is that the population has outgrown the food supply. there is also evidence that the currents passing through the whales migration route has become less suitable for amphipods.
lee cooper, an ecologist at the university of maryland, told new scientist magazine: "there is also evidence that the overall productivity of the northern bering sea [on the whales' migration route] has declined over the past 10 to 20 years.
"in my view, the stinky whales may be facing a food shortage."
the eastern north pacific grey whale was almost hunted to extinction in the 17th and 18th century prompting a ban on hunting the mammals in 1946.
aboriginal hunters - the chukchi people of siberia and the makah people of washington state - are now allowed to kill 140 of the whales between them each year.
chukchi hunters first noticed a problem in the late 90s although elders say the problems stretched back to the 60s and 70s and they now claim that ten per cent of the whales are inedible.
gennady inankeuyas, chairman of the association of traditional marine mammal hunters of chukotka, said: "the smell reminds me of medicine tablets, and nobody can eat the meat."
interesting study, they didn't mention the outstanding feature of it, which is, an intramuscular vaccine injection followed by an oral dose is not effective while the other way around - orally followed by intramuscularly - is effective
that is, the digestion must tag its products so that the immune system doesn't react against them once in the blood
if you have food allergies there is a major dysfunction with tagging not occuring or being overwhelmed or lacking discrimination, probably some dairy peptides are intrinsically difficult to descriminate
strongly associated with biofilm toxin disruption and deliberate suppression of immune function by the biofilm i'd say
New immunization methods offer long-term protection against H. pylori in humans and may contribute to a possible ulcer vaccine in the future say researchers from the University of California, Davis. They report their findings in the July 2007 journal Infection and Immunity.
Helicobacter pylori is a bacterium that colonizes the digestive tract of 50% of the world’s population. Infection commonly occurs in early childhood and can lead to chronic gastritis, peptic ulcer disease and gastric cancer throughout the life of its host. Antibiotics are currently used against H. pylori infection, however increasing resistance as well as high treatment costs and recurrence of infection emphasize the need for an effective, long-lasting vaccine.
In the study mice were immunized in four groups: orally alone, intramuscularly alone, orally followed by intramuscularly, and intramuscularly followed by orally and then challenged orally with H. pylori after three months. Results showed that mice receiving intramuscular immunization alone or a combination of oral and intramuscular vaccinations had significantly reduced bacterial loads and no detectible H. pylori in the intestinal tract. Mice immunized orally alone or intramuscularly followed by orally were not protected and had decreased antibody responses.
“This study demonstrates the ability to induce long-term immunity against H. pylori, provides correlates of protection, and illustrates the crucial role of the immunization route(s),” say the researchers.
(J.M. Taylor, M.E. Ziman, J. Fong, J.V. Solnick, M. Vajdy. 2007. Possible correlates of long-term protection against Helicobacter pylori following systemic or combinations of mucosal and systemic immunizations. Infection and Immunity, 75. 7: 3462-3469).
"Biofilms, formed by bacteria's such as Pseudomonas, are a slimy matrix which includes proteins, sugars and DNA, all produced outside the bacterial cell.
These structures enable bacteria to survive on all kinds of surfaces and protect them from antibiotics and immune system attack. They are believed to prevent the successful treatment of Pseudomonas aeruginosa in the lungs of cystic fibrosis (CF) patients.
The researchers found that the DNA in the matrix was the key to its structure.
"This is the structural glue of the biofilm," said Dr Whitchurch (University of Queensland's Institute for Molecular Bioscience)
The researchers then found that an enzyme called DNAse 1 – which breaks down DNA – can be used to break down biofilms and prevent their build-up in the first place.
The DNA in biofilm had been ignored because it was thought to be dead bacteria. Dr Whitchurch initially thought that sugars were the glue in the PS biofilm.
But when this line of research met a dead end, she re-discovered old reports that showed DNA was deliberately produced by the bacteria in their 'slime'. This was when she realised the DNA might be the structural key to the biofilm."
above from article
my comment: the 'mould' issues that seem to be very in vogue may in fact be cystic fibrosisy biofilm growth in the lungs in damp cold (maybe warm damp as well) spore laden air
it gets more interesting (see clipping/quote below this section)
the bacteria scavange dna and actin from neutrofils for the biofilm and this could be a BIG factor in intractable gut infections, nice positive feedback loop for a major disaster
also supplementary yeast and even vegemite as a dna/rna source may be an issue, as i notice too much vegemite promotes biofilm
would be why selenium yeast never seems right
chromium yeast may not be an issue because of chromiums effect of breaking dna hence some toxic effect with the uptake of the chromium yeast nutrients on the bacteria in a similar manner to cynacobalamin
might be a problem with yasko's rna supplements too
since the immune systems response to viral stress reduces its capabilities against bacteria, low viral impress/infection enviroments will be extremely important to ibs/colitis/chron's sufferers and for those less affected in the gut, there could be a bad neural impact from biofilm toxins
so bacteria just don't eat dna, they can use it as a biofilm building block
" Researchers believe that Pseudomonas establishes a chronic infection in the airway of CF patients by creating a biofilm, a three-dimensional structure composed of bacteria encased in an extracellular matrix. Other examples of bacterial biofilms include the plaque that forms on teeth and the "slime" that forms on rocks in a stream. Bacteria in biofilms take on distinctly different characteristics from those floating free in a "planktonic" form. Once Pseudomonas develops a biofilm it becomes significantly more resistant to both antibiotics and the immune system.
The immune system attempts to eradicate Pseudomonas by sending in massive numbers of cells called neutrophils. The short-lived cells die after a short time and cellular debris accumulate in the airway of CF patients.
In a series of experiments with neutrophils and Pseudomonas, Dr. Nick and his colleagues found that the contents of dead neutrophils, particularly DNA and a filament called actin, provide a scaffolding for Pseudomonas to construct a biofilm. In the presence of neutrophils, the development of P. aeruginosa biofilms increased by two and a half to three times compared to P. aeruginosa cultures without neutrophils "
“ The researchers found strong fungal-bacterial interactions in those with Crohn’s disease : two bacteria (Escherichia coli and Serratia marcescens) and one fungus (Candida tropicalis) moved in lock step.
The presence of all three in the sick (ed. crohn's) family members was significantly higher compared to their healthy relatives, suggesting that the bacteria and fungus interact in the intestines. the three work together (with the E. coli cells fusing to the fungal cells and S. marcescens forming a bridge connecting the microbes) to produce a biofilm — a thin, slimy layer of microorganisms found in the body that adheres to, among other sites, a portion of the intestines — which can prompt inflammation that results in the symptoms of Crohn’s disease ”
S. mother of a 3yr old boy, ASD, began SCD Feb, 2007 writes:
Yesterday the sandy, gritty poo...today the sandiness is gone but about 10 "things" were there. They were all different shapes from round to seed shaped. About 1/4" in diameter and plump and goldish in color. The only thing I can think of are raisins that have been rehydrated from being in his system. The other thing is that I know for a fact that he hasn't had any raisins for 1 month because he has been with me constantly and we have no raisins in the house and we haven't been anywhere where there were raisins. I know he had some appx 1 month ago, maybe 6 weeks. But I really don't look like raisins, it's just the closest thing I can come up with. Does anyone know what these "things" could be?
she writes again in reference to the photos below:
Thank you so much! Those pictures definitely look like what my son had. I googled yeast ball, Candida tropicalis and ended up with aspergillum or something like that. It is way too complicated for me. I have for 2 days been giving Benito the carrot juice and garlic anti fungal so I am assuming that it's working because it literally kicked them out.
the photos below are from sasha's recovery photos on yahoo
On Sabouraud's dextrose agar colonies are white to cream colored, smooth, glabrous and yeast-like in appearance. Microscopic morphology shows spherical to subspherical budding yeast-like cells or blastoconidia, 3.0-5.5 x 4.0-9.0 um in size.
India Ink Preparation: Negative - no capsules present.
Cornmeal and Tween 80 Agar Plate: Abundant long, wavy, branched pseudohyphae with numerous ovoid blastoconidia budding off. Terminal vesicles (chlamydoconidia) are not produced. Fermentation Reactions: Where fermentation means the production of gas and is independent of pH changes.
Positive: Glucose; Maltose; Galactose; Trehalose (delayed).
Positive: Glucose; Galactose; Maltose; Trehalose; D-Xylose; Soluble Starch; Succinic acid; D-Mannitol; L-Arabinose (weak); D-Glucitol.
Variable: Sucrose; Salicin; Melezitose; Glycerol; Cellobiose; D-Ribose; Ribitol; L-Sorbose; Citric acid; DL-Lactic acid.
Negative: Potassium nitrate; L-Rhamnose; Lactose; Raffinose; Melibiose; Galactitol; Erythritol; Inositol; D-Arabinose.
the above from this article
my comments on the above :
look at the fermentations and all the scd illegal sugars Candida tropicalis assimilates
interestingly it assimilates glucose which is a single sugar, and really is a verification of the biofilm carbohydrate diet (BCD) principles
you can see that mechanically such large biofilms have the ability to impede the intestines absorption of simple sugars and grab them first
candida tropicalis is naturally part of the mucocutaneous gut wall
if the photos are candida tropicalis they seem to afix through damaged mucosal wall and need some immune supression to thrive and maybe a lack of gut wall motility
candida tropicalis seems to do well on scd illegal sugars so i guess they must be doing ok on the smaller amount of cross linked sugars available in in scd legal vegs and fruits
i think this is where you get into a more biofilm oriented diet like bee wilder's candida diet or low carb/high fat scd
the BCD in addition uses digestive enzymes and promotes the immune system
“ something weird in floating in toilet after BM
but when I stood up to wipe, there was a weird egg (scaled photos are in cm) thing floating in the toilet, separate from the poo
I didn't feel anything abnormal pass, but there was nothing in the toilet before I went so I am assuming it came from me : o (
I'm not sure if it is vaginally or rectally derived material, but there was no associated pain
It is mostly yellow and fairly firm. There look to be some white veins and some red patches
of note, on one of the ends there is an area that looks even more red/brown/and texturized
I have never seen or heard of anything like it before and it is thoroughly freaking me out! I'm a 23 year old female in relatively good health, although I have been under a lot of stress recently and my diet has been pretty poor (lots of energy drinks and coffee and definitely not enough food…I'm probably underweight at 5'8" and 115lbs)
I'm not currently on any medication, but went off birth control (Yaz) in January
I had a period in late March after going off Yaz and it seemed normal. This was the first period I'd had in probably 5 years, I had been on Yaz for about 7 years but my period waned after awhile) ”
“ the day before yesterday I had a large amount of diarrhea, and found some questionable 'peanut' shapes in my stool, as well as what looked like mucus and odd brown gelatin-like shapes
interesting study below, shows how yeast can change to match biofilm needs, lots of potential for mutation
no wonder they are so hardy
what's interesting about the yeast is the way they get extra chromosomes or double up, which is basically turning everything on more, they can get more viralent if the conditions are right
the weaker one gets, the more they can go to town
even healthy bods can be taken, good nutrition feeds yeast, we are always on the edge of a more severe yeast infection
yeast missing sex genes undergo unexpected sexual reproduction (may 2009, duke university medical center)
an emerging form of the pathogenic yeast candida is able to complete a full sexual cycle in a test tube, even though it's missing the genes for reproduction. and it may also do so while infecting us
sex contributes to the candida yeast species' evolutionary success, i think the fact that it has a complete sex cycle is likely to play a role in the evolution of drug resistance in this emerging pathogenic yeast species.
yeast infections are notoriously hard to treat and yeast are one of the most successful pathogens and commensals in nature. a commensal is an organism that benefits from associating with another organism without affecting the other. humans are susceptible to three types of yeast infection: thrush (in the mouth and throat), vaginal infection, and a sometimes fatal systemic infection of bloodstream and organs, such as the kidney.
eight candida species which have a sexual cycle were missing many of the genes related to reproduction found in other species.
the unrecognized sex cycle could mean we need to develop new treatments to combat what is really happening in humans infected by yeast.
how could the yeast sexually produce spores when they lack so many genes responsible for meiosis, the process of sexual cell division that reduces chromosomes to half their number in the progeny?
by examining and defining the structure and functions of the mating-type genes in yeast, it was learned that forms of candida yeast undergo meiosis but generate offspring of several types. about two-thirds have the classic 50:50 division of chromosomes from the split parent cell, but a third of them have an extra chromosome or even double copies of all chromosomes.
"what we found is that the sexual cycle has a new way to create genetic diversity, and it provides a unique vantage point from which we can explore the mechanisms of sexual reproduction. this provides a new way to study sexual reproduction and how chromosomal abnormalities arise."
candida's meiosis without meiotic genes may be what gives rise to the progeny with unusual numbers of chromosomes. or maybe the genes were lost for a reason, to provide a route to genetic diversity. or maybe these differing types of progeny are the unfortunate consequence of undergoing meiosis without the machinery that species normally have when they reproduce sexually.
humans, too, have their share of oddly paired chromosomes. experts estimate that about 10 to 30 percent of human eggs or fusion products may be aneuploid, with chromosomes from mother and father not paired exactly one to one, but the great majority of those fusions of sperm and egg don't make it to the implantation and pregnancy stage. that's why it is important to find models like this, so that we may shed light on related human conditions.
"Prior to this we've believed that fungi were generally confined to vertical gene transfer or conventional inheritance, a slower type of genetic change based on the interplay of DNA mutation, recombination and the effects of selection," said Michael Freitag (Oregon State University).
"But in this study we found fungi able to transfer an infectious capability to a different strain in a single generation," he said. "We've probably underestimated this phenomenon, and it indicates that fungal strains may become pathogenic faster than we used to think possible."
Bacteria use "horizontal" genetic transfer through chromosomes and DNA plasmids to change quickly, which is one reason that antibiotic resistance can often develop. This capability was believed to be possible, but rare, in fungi. In the new study, based on a genome-wide analysis of three Fusarium species, it was shown experimentally that complete chromosomes were being transferred between different fungal strains, along with the ability to cause infection. Various Fusarium fungi can infect both plants and humans.
In humans, fungal infections are less common than those caused by bacteria, but can be stubborn and difficult to treat – in part, because fungi are far more closely related to animals, including humans, than are bacteria. That limits the types of medical treatments that can be used against them. Fungal infections are also a serious problem in people with compromised immune systems, including AIDS patients, and can be fatal.
On a more basic level, this study provides evidence that the "tree of life," with one trunk and many branches, is outdated. It should be replaced by a "network of life" in which many horizontal connections occur between different species.
there's been a recent study by cornell university in ithaca (july 2007) examining small intestine inflamation which i guess they are calling crohn's
they didn't find mycobacterium avium paratuberculosis (MAP), but they found e.coli with plenty of other pathogen horizontal gene transfer, strange genes like from the plague bacterium, in the e.coli
classic biofilm mutation with heaps of stealth tailored to the individual immune system i bet which would be why it's such a difficult condition to eradicate
the ileum has an excellent blood supply (transporting digested food molecules to the liver) so the biofilm toxins must readily distribute to the brain, especially if liver function is also impaired by the biofilm toxins
there is a double whammy with viral exposure deprecating liver detox function, allowing more biofilm toxins to flow onto other organs and the brain
this would explain the mentally and hormonally cacked condition so typical of ibs and crohns (brains being fryed as well as straight neural starvation) and also the power of the biofilm carbohydrate diet™ in improving intellectual performance since it would deprecate such toxins
scd does not appear to cut the bill since the behavior of the people doing it is so toxic
new scientist article:
CROHN'S disease might be caused by bacteria that have borrowed a few nasty genes from, of all things, plague.
Crohn's is an incurable inflammation of the intestine that affects 1 in 1000 people in Europe and North America. Researchers suspected gut bacteria were to blame, but could not be sure which, as tests often produced contradictory results. Now Ken Simpson and colleagues at Cornell University in Ithaca, New York, have discovered a possible reason for the confusion.
When they studied bacteria from the guts of people with inflamed small intestines, they found no evidence of MAP, a bacterium that some have blamed for Crohn's. MAP is related to the TB bacterium.
However, they did find higher than normal levels of the common gut bacteria E. coli in more inflamed areas. These E.coli uniquely carry disease-related genes from a host of other pathogens, including salmonella, cholera and bubonic plague, as well as from strains of E. coli that cause disease outside the gut (The ISME Journal, DOI: 10.1038/ismej.2007.52).
(ileum: part of the small intestine of the digestive system, between the duodenum and the colon, that absorbs digested food)
Intestinal bacteria are implicated increasingly as a pivotal factor in the development of Crohn's disease, but the specific components of the complex polymicrobial enteric environment driving the inflammatory response are unresolved. This study addresses the role of the ileal mucosa-associated microflora in Crohn's disease. A combination of culture-independent analysis of bacterial diversity (16S rDNA library analysis, quantitative PCR and fluorescence in situ hybridization) and molecular characterization of cultured bacteria was used to examine the ileal mucosa-associated flora of patients with Crohn's disease involving the ileum, Crohn's disease restricted to the colon (CCD) and healthy individuals . Analysis of 16S rDNA libraries constructed from ileal mucosa yielded nine clades that segregated according to their origin (P<0.0001). 16S rDNA libraries of ileitis mucosa were enriched in sequences for Escherichia coli (P<0.001), but relatively depleted in a subset of Clostridiales (P<0.05). PCR of mucosal DNA was negative for Mycobacterium avium subspecies paratuberculosis, Shigella and Listeria. The number of E. coli in situ correlated with the severity of ileal disease ( 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum.
in other words, enzymes are not enough, you have to do biofilm scd as well
lovely to have to research for this, even if the journalist and researchers are glycemic index twits
THE STRUCTURAL BASIS OF THE SLOW DIGESTION PROPERTIES OF THE NATURAL CEREAL STARCHES.
"Starches can be divided into three groups: rapidly digestible starch (RDS, digested within 20 minutes), slowly digestible starch (SDS, digested between 20 and 120 minutes), and resistant starch (RS). The latter is not digested but is fermented in the large intestine and has ‘prebiotic' properties.
Lead author of the two studies, Genyi Zhang from the Southern Yangtze University in China, reports that maize starch (Tate & Lyle) consists of 53 per cent slowly digestible starches, with 22.4 per cent RDS, and 22.6 per cent RS. Potato starch consists of only 15 per cent SDS, he said.
Using X-ray powder diffraction and scanning electronic microscopy (SEM) the researchers determined that high proportion in SDS in the maize was associated with the A-type crystalline structure, as opposed to the B-type in potato starches.
“These observations demonstrate that the supramolecular A-type crystalline structure determines the slow digestion property of native cereal starches,” wrote the Southern Yangtze University and Purdue University researchers.
In other words, it is this specific internal structure that delays digestion and conversion into glucose, and is the reason behind the slow digestion of the starches. Expansion of this criteria could lead to the identification of other SDS that could lower the GI of foods.
The researchers also suggested ways of forming slow digestible starches: “This study indicates that a SDS material can be made by encapsulating easily digestible material, for example, gelatinized starch, between layers of films that are resistant to enzyme digestion, and food products with multiple layers of this structure would likely have a slow digestion property.”
STARCH AND PHOSPHORYLATION
molecular mechanisms of starch breakdown in plants
Energy from the sun and carbon dioxide fuel photosynthesis in plants and algae, making life on earth possible. Carbon that is fixed by plants is converted to starch and sucrose, which are utilized by plants for energy and to build biomass. Human evolution and society have been intimately tied to our exploitation of plant biomass for food, fuel, tools, and shelter. However, to be usable, the starch carbohydrate stored in plants must be broken down to component sugars. Some aspects of starch metabolism have been known for many years, but regulation of the process and exact physical mechanisms are still not well understood. With new information emerging from genome sequencing and mutational analyses, we are beginning to gain a better understanding of these complex and finely tuned processes. Such knowledge is especially critical as we struggle with issues of energy and food supply.
Some of the new molecular mechanisms and regulatory components in starch metabolism have been identified by Dr. Samuel Zeeman and his colleagues. Dr. Zeeman, of the Institute of Plant Sciences, ETH Zurich, in Switzerland, who is the 2007 recipient of the Charles Albert Shull Award, will be presenting this work at the opening Awards Symposium of the annual meeting of the American Society of Plant Biologists in Mérida, Mexico (June 27, 2:30 PM). Mutational and structural analyses by Dr. Zeeman and his colleagues have revealed that starch degradation in Arabidopsis leaves at night differs significantly from the versions traditionally described in textbooks. Specifically, mutations at the Starch Excess 4 (SEX4), Maltose Excess 1 (MEX1) and other loci produce plants unable to metabolize starch to a usable form.
When we use starch in the lab or cook with it, we tend to think of it as an amorphous mass, but it is really a complex, ordered substance. Starch consists of two polysaccharides (polymers of the simple sugar glucose) -- amylopectin and amylose. Both are long chains of connected glucose molecules, but amylopectin is also highly branched and forms a tree-like structure. The branches are then packed so that double helices can form between the chains, which are arranged into concentric layers forming semi-crystalline starch granules. This exquisite structure is extremely stable to enzyme activity and can thus be stored by the plant for later use. However, when needed, starch must be broken down to its component sugars for export to the rest of the plant. It appears that a number of proteins are major players — debranching enzymes, glucanotransferases and amylases, among others -- and that in leaves, their actions are finely tuned to the diurnal changes in photosynthesis and the circadian rhythms of the plant.
Some of the new proteins that have been identified by Dr. Zeeman and other researchers in the field act as glucan kinases and phosphatases, that is, they place and remove phosphate groups on the starch molecules. Among these proteins are glucan water dikinase (GWD), phosphoglucan water dikinase (PWD) and SEX4. It is thought that GWD and PWD act in concert to place phosphate groups on starch molecules. The highly charged phosphate group may act as a wedge, disrupting the semi-crystalline packing in the starch and allowing degradative enzymes access to the glucose chains and branches. SEX4 then removes the phosphate groups. Although the exact mechanisms of how these proteins coordinate starch metabolism are still unknown, the importance of phosphate groups in the process is now well established. Mutants of all of these proteins result in plants with an excess of undigested starch.
Sequencing analyses have shown that GWD is conserved over many plant taxa, and proteins similar to SEX4 have been found in other plant species, including rice, maize, and tomato. The amylopectins of leaf starches in different plant species have also been found to be decorated with phosphate groups. Studies of Arabidopsis and potato leaves suggest a common mechanism for starch breakdown, although different pathways may operate in other plants. Further research is needed to establish conservation of the process as well as the proteins in the plant kingdom.
Elements of the newly-discovered mechanism of starch breakdown may also be conserved across kingdoms. Amylopectin has similarities to glycogen, the soluble storage carbohydrate accumulated in animals, fungi, and bacteria. The SEX4 phosphatase is related to laforin, a protein involved in animal glycogen metabolism. When laforin is missing, insoluble starch-like polyglucosans (Lafora bodies) accumulate, which results in neuronal dysfunction, severe epilepsy, and death. The similarities between the animal and plant processes suggest common regulatory mechanisms, which may be the result of evolutionary convergence or conservation.
a healing crow thread titled "diarrhea/intro diet - try low carb"
As Anne said, 24 hour yogurt is fine, but strain it.
I think it is the lactose in the dairy that is the problem for people, and that is removed by fermentation. Hard cheese and butter should be fine.
Why did the nutritionist say no hard cheese? Ask for scientific reasons.
I have been on the scd for a few years. I didn't get better until I went on a high fat no carb. version. Look up Aitkins diet for tips on how to get into ketosis and test urine with ketosticks from the chemist. So definitely no fruit or honey and only green veg. It is worth a try.
I was VERY depressed getting through the carb. withdrawal but have never been better in the 2 years since I have been doing it.
I'm glad you found someything that worked for you but Elaine did not want SCD to be generally used or interpreted as a low carb diet and certainly not to be confused with Atkins.
Although a low carb diet can be effective for siezures, it can lead to ketosis.
SCD has always been about the TYPE of carbs not the amounts. So I suggesting to others, unless you have an unusual condition like Christine's include adequate amounts of legal carbs in your menu.
Also SCD is not intended to be a weight loss diet although it usually stabilizes weight once a healthy one is attained. This happened in my case. i had lost 86 pounds before starting SCD and have stayed at an appropriate weight for my height and age for the past six years and eaten very well on SCD.
my reply :
if you work biofilms into scd then you understand that scd can be low carb
high fat and no fruit or honey and only green vegs is quite a valid scd approach if you are not going to use enzymes and fits the theory if you include biofilms
there are other issues with fruit too, including yeasts spores, but cooking can help with that
it would be wonderful if elaine were alive and able to persue the implications of biofilms for scd, indeed it was her interest in the subject i remember from when she was posting several years ago that has made me look closer, but she is no longer with us and in the same as as scd moved on from sidney haas, so scd is moving on from elaine.
there is no necessity to move into ketosis though, in fact with judicous supplementation to maximise the bodies natural fat metabolism, particularly chromium gtf, it can be avoided.
there are actually several versions of scd around, sidney haas's, eliane gottschal's btvc and also i feel pecan bread is a bit different from btvc and i have a revision including updating the theory to include biofilms
also with high fat you need to supplement fish oil and maybe an organic sunflower oil, or at least use them to balance up the saturated fats
a healing crow thread titled 'low carb scd' (august 06)
Doing a low carb version of SCD is the only thing that has ever worked for me as well. Trust me, I would rather be eating the fruit/honey even in moderate amounts, but I have experimented back and forth enough to know that if I stay low carb, I am much better off.
this low carb thing points to a flaw in the btvc scd
the btvc scd uses the erronous free floating gut flora model
that is it supposes that the flora are not anchored in the gut and all you have to do is starve them
but actually they are sheltered in the gut in biofilm which is basically a sugar structure and reasonably persistent especially if you are still providing simple sugars to the the diet with btvc scd legal fruits and veges
the only way to get around this is to eliminate carbs almost completely or use enzymes
Actually, I would disagree with you and say one of the flaws in BTVC thinking is that it assumes that all gut pathogens ARE anchored in the gut, and specifically I think Elaine made the assumption that they were all to be found in the large intestine, not in the small intestine, or stomach, or mouth or wherever else they eventually get to.
For example, the whole premise that honey and fruits are ok because they are a simple sugars that are quickly digested in the stomach before the pathogens can get to them in the colon, I find seriously flawed. Many of us can feel the fermentation of these sugars within an hour to 3 hrs of eating them which means the pathogens are in the stomach (0-2 hrs) or small colon (2-5 hrs). Also, even mainstream medecine has come to acknowledge the studies showing the strong correlation between pathogens in the SMALL bowel and IBS where antibiotic therapy has been used very successfully (See Dr. Pimental's work at Cedar Mt Sinai Hospital in LA). Also, Elaine never bought into the concept of candida overgrowth, let along systemic candida throughout the body (yeast infections, sinus infections etc.).
But she did believe in the concept of a biofilm...
i have occasionally seen descriptions of what looks like an unanchored biofilm in the stomach from web posts
capsule type objects that are not supplements or known parasites that are part of the stomach contents from vomiting
thats an interesting insight u have that btvc is targeted at the lower bowel with its removal of the slower fermenting complex sugars but not targeted at the stomach or upper bowel
biofilm in the upper colcon could well get to the simple sugars first and be actually able to impair absorbtion of them
elaine understood the implications of biofilm but it never got worked into a new scd theory which is what would have happened if she had been younger
the trouble with fruits is not just the sugars of which a portion are complex as well as simple, but that they are loaded with live yeast and other biofilm components and spores, i find pan frying of any fruit in beef fat i eat very effective for reducing this
some recent research (2006) in the context of the ketogenic diet and low brain cell levels of glucose, imply that the transcription factor NRSF is bound by CTBP and and a bevy of neuronal genes are no longer switched on which is how the ketogenic diet works
but in the normal context, brain cell glucose is necessary to bind CTBP thus leaving NRSF unbound and turning on neuronal genes
the upshot as far as scd and biofilm_scd is that eliane gottschall was right and fruits and carbohydrates are necessary to ensure that the brain is kept out of the ketogenic downregulated neuronal gene function area.
scd and biofilm_scd are not protein only diets, but deliver fruit, dairy and vegetable sugars to the brain.
"Avtar Roopra has long explored how certain proteins known as "transcription factors" turn neuronal genes on or off. He has been particularly intrigued by one transcription factor known as NRSF, which is thought to control up to 1,800 genes in the brain, including many that are implicated in epilepsy. Like an electrical motherboard, NRSF ensures that neuronal genes switch "on" in the body's neurons, while remaining switched "off" in other regions where they normally play no role.
Roopra found that NRSF binds to another protein called CTBP. The finding "immediately raised alarm bells," Roopra says, because CTBP also binds to a free-floating molecule - NADH - that emerges when sugars break down in cells. To his surprise, Roopra found that CTBP binds to either NRSF or NADH. In other words, a cell with a lot of glucose generates a lot of NADH, so CTBP is more likely to bind with the sugar byproduct than NRSF. But without CTBP, NRSF most likely derails the normal function of certain neuronal genes - including those connected to epilepsy"
University of Wisconsin-Madison
more on biofilm
so biofilms forming on food particles means that yogurt is a biofilm,
just devoid of large scale structural features
when it invades the mucosa getting through to the underlying layers of tissue is bad news i think and what gives the bad reaction to enzymes
so even in terms of straight scd with its concern for complex sugars, biofilm is instrumental as biofilms would form around the food particles with complex sugars in
"Mucosal and other biofilm populations in the large gut
Biofilms are communities of microorganisms which form at phase interfaces and exhibit phenotypes profoundly different from those of identical microorganisms in suspension. Properties of biofilm include a enhanced resistance to antimicrobial treatment, persistence in extreme environments, enhanced resistance to immune effector elements and increased propensity for gene transfer. Biofilms contribute to a number of medical conditions; for example, cystic fibrosis, burns, ulcerative colitis, endocarditis and indwelling device-associated infection.
Transmission electron micrograph of a biofilm of unusually long spiral shaped bacteria on rectal mucosal biopsy.
The gastrointestinal tract is an ideal location for biofilm formation. There is present a large surface area, high levels of nutrient and a diverse and dense indigenous microflora. In the gastrointestinal tract biofilms are attached to food particles in the lumen, to the mucosa and can be found within the mucous layer. Microbial communities associated closely with the mucosa are important because of their ability to interact with the host tissues and thus influence the health of the individual.
In our laboratory we are interested in biofilm formation primarily in the mucous layers of the rectum and colon and on PEG tubes and the gastric mucosa of enteral tube-fed patients"
sIgA contrbutes to the adhesion of E. coli to epithelial cells
so biofilm is really part of the gut and u can see how a skewed immune system say over producing sIgA woudl lead to excessive anchoring by some bacteria and hence biofilm
i really think its this excessive anchoring that is the bad news and enzymes are able to attack the anchoring directly
biofilms may well be able to skew the immune system to suit themselves
a high fat/very low carb diet would also profoundly modulate, really an extreme of scd since energy in fat form is not very accessable to gut bacteria and flora
Human secretory immunoglobulin A may contribute to biofilm formation
in the gut. Bollinger RR, Everett ML, Palestrant D, Love SD, Lin SS, Parker W.
Departments of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
It is critical, both for the host and for the long-term benefit of the bacteria that colonize the gut, that bacterial overgrowth with subsequent bacterial translocation, which may lead to sepsis and death of the host, be avoided. Secretory IgA (sIgA) is known to be a key factor in this process, agglutinating bacteria and preventing their translocation in a process termed 'immune exclusion'. To determine whether human sIgA might facilitate the growth of normal enteric bacteria under some conditions, the growth of human enteric bacteria on cultured, fixed human epithelial cells was evaluated in the presence of sIgA or various other proteins. Human sIgA was found to facilitate biofilm formation by normal human gut flora and by Escherichia coli on cultured human epithelial cell surfaces under conditions in which non-adherent bacteria were repeatedly washed away. In addition, the presence of sIgA resulted in a 64% increase in adherence of E. coli to live cultured epithelial cells over a 45-min period. Mucin, another defence factor thought to play a key role in immune exclusion, was found to facilitate biofilm formation by E. coli. Our findings suggest that sIgA may contribute to biofilm formation in the gut.
since breaking down a biofilm may release bacteria into their free living state a synergisitc approach with supplements, diet aka BCD and high fat, and protease and polysaccharide enzymes may be necessary
a single sugar dissolving enzyme may only be partially effective and supplementing and oral/skin d to correct immune system skew as well as a BCD higher fat diet being required
there appear to be biofilm "communication disruptors" in laboratory development
Bassler's group also found that quorum sensing squelches cholera biofilm formation by turning off polysaccharide production at high cell density.
cholera's quorum-sensing system also suppresses biofilm formation. At the molecular level, the signal transduction pathway turns off the Vibrio polysaccharide synthesis (vps) operons that make the sticky matrix for biofilms. Quorum sensing also triggers a protease known to detach cells, perhaps both from the epithelial lining of the intestine and from biofilm aggregations. "Quorum sensing lets the bacteria leave the biofilm at the right time to find new opportunities after infection," Zhu said.
http://focus.hms.harvard.edu/2003/Nov21_2003/microbiology.html also health/biofilm/cholera life cycle.htm
no wonder the stones keep coming with liver/bile flushes, they are being made by biofilm all the time
"Pathogenic bacteria commonly produce a thick, mucous-like, layer of polysaccharide. This "capsule" cloaks antigenic proteins on the bacterial surface that would otherwise provoke an immune response and thereby lead to the destruction of the bacteria"
"The Organic-Mineral Interface in Bone Is Predominantly Polysaccharide" erica wise et al
bone is a complex composite of sugars, glycoprotiens and minerals
glycosaminoglucan which is a long unbranched polysaccharide, binds the collagen to the minerals in bone
no wonder plaque can just cut through teeth, just enzymases the polysaccarides binding the collagen to the mineral phases
biofilm will be doing a similar stitching with proteins/glycoproteins and polysaccharides to form gall and kidney stones
the fundamental point is these stones are not formed in test tubes as pure uncatalysed chemical/mineral reactions but are actively mediated by biofilm enzymatics
"Hultgren first discovered that bacteria are able to invade bladder cells in 1998, he later found evidence in his animal model that bacteria could establish residence inside those cells. He showed that this process involved several behavioral changes that allow the bacteria to form cooperative communities known as biofilms. By working together, bacteria in biofilms build themselves into structures that are more firmly anchored in infected cells and are more resistant to immune system assaults and antibiotic treatments.
To prove that the model correlates with human infections, Rosen led an analysis of human urine samples sent from a clinic at the University of Washington in Seattle. The 100 patients who gave samples were either suffering from an active, symptomatic infection or had previously suffered infections. Researchers analyzing the specimens were not told which group of patients individual specimens had come from.
Using light and electron microscopy and immunofluoresence, scientists found signs of bladder cell infection in a significant portion of the samples from patients with active UTIs. These included cells enlarged by bacterial infection and shed from the lining of the bladder.
In addition, Hultgren's experiments had previously suggested that some bacteria progress to a filament-like shape when exiting out of the biofilm. Rosen was able to identify bacteria with this filamentous morphology in 41 percent of samples from patients with symptomatic UTIs.
Neither indicator was detected in urine from women who did not have active infections. This was anticipated: Hultgren's animal model work suggests that when women are between episodes of symptomatic infection, intracellular E. coli may be in dormant phases where there would be little cause for bacteria or the cells they infect to be shed into the urine."
senior author Scott J. Hultgren, Ph.D., the Helen L. Stoever Professor of Molecular Microbiology at the School of Medicine, Washington University, St. Louis
an openblooms thread (august 06)
Some months ago when I was looking up c-diff for a friend, I came across a web site that said the reason that c-diff is so hard to eradicate is that it uses spores to generate a new generation. So you kill off the adults, but the spores hibernate until the gut is more favorable to growth, when they start growing again. So you go back on the antibiotic, kill the adults, and the spores wait again.
This particular doctor's theory was to go on the antibiotic until the diarrhea stops. Then 2, 3, or 4 days later, when it begins again, to go back onto the antibiotic. Some people may need to do this for months, depending on how entrenched the problem is. Hopefully, you eventually catch the spores before they can generate more, and the infection is gone.
if saccharomyces is an assist to defeating clostridia then its likely that clostridia is in a biofilm synergy with another yeast type (candida is a good biofilm former whereas saccharomyces cerevisiae is not) and also biofilm provides physical protection against antibiotics and the immune system
the saccharomyces may help displace the clostridia yeast synergent, possibly in part by uncloaking an immune response to yeast
oreganol and candex may be an assist to an antibiotic
with biofilms, the bacteria provide the enzymes, the yeast the anchoring and the viruses the immune system defeat
vitamin d promotes pathways providing anti-bacterial peptides
since c.diff is never wiped out and goes to spore form, getting the immune system functioning is the only long term solution to controlling it
1. Saccharomyces boulardii is a nonpathogenic yeast that releases a protein that interferes with the binding of toxin A to its receptor (17).
2. Cerevisae may be even better
3. Lactobacillus GG and other probiotics help repopulate and control the population of c. difficile.
4. Remember, c.difficile can also live on protein, therefore reducing available carbohydrate alone may not control it. The yoghurt should definitely be key.
5. Clostridia is an anerobe, so good oxygenation is necessary to keep it under control. Therefore, anemic or low iron conditions to be avoided. Include foods high in iron. Plus other compendium supplements.
I am sorry I don't have the studies to link to here, did not save them I guess. But, from my summary above I remember that there were studies on cerevisae that seemed to suggest that it was non invasive as well as non toxic. I did come across a couple of mentions from researchers recommending that more studies need to be done on the invasiveness and possibility of pathogenesis of s.boulardii.
moreover, s. boulardii works by neutralizing the effect of toxin A, whereas it does not do anything for Toxin B or for eliminating the bacteria itself.
here is a good link for clostridia:
interesting that is was the 'cerevisiae' that was a poor biofilm former in the following research
Chandra J, Kuhn DM, Mukherjee PK, Hoyer LL, McCormick T, Ghannoum MA.Chandra J, Kuhn DM, Mukherjee PK, Hoyer LL, McCormick T, Ghannoum MA.
Center for Medical Mycology, University Hospitals of Cleveland, and Department of Dermatology, Case Western Reserve University, Cleveland, Ohio
Biofilms are a protected niche for microorganisms, where they are safe from antibiotic treatment and can create a source of persistent infection. Using two clinically relevant Candida albicans biofilm models formed on bioprosthetic materials, we demonstrated that biofilm formation proceeds through three distinct developmental phases. These growth phases transform adherent blastospores to well- defined cellular communities encased in a polysaccharide matrix. Fluorescence and confocal scanning laser microscopy revealed that C. albicans biofilms have a highly heterogeneous architecture composed of cellular and noncellular elements. In both models, antifungal resistance of biofilm-grown cells increased in conjunction with biofilm formation. The expression of agglutinin-like (ALS) genes, which encode a family of proteins implicated in adhesion to host surfaces, was differentially regulated between planktonic and biofilm- grown cells. The ability of C. albicans to form biofilms contrasts sharply with that of Saccharomyces cerevisiae, which adhered to bioprosthetic surfaces but failed to form a mature biofilm. The studies described here form the basis for investigations into the molecular mechanisms of Candida biofilm biology and antifungal resistance and provide the means to design novel therapies for biofilm-based infections.
We have isolated 6 morphologically different axenic yeast cultures from the film surface of red wine. Based on morphological, physiological and biochemical characteristics we have identified the strains as follows: isolates 1-4 are morphologically different strains of the anamorph basidiomycetous film-forming yeast Candida humicola (DASZEWSKA) DIDDENS et LODDER, syn. Apiotrichum humicola (DASZEWSKA) VON ARX WEISMAN. Isolates 5 and 6 belong to the genus Saccharomyces of the associated species S. cerevisiae (isolate 5 originally S. bayanus, isolate 6 S. capensis). These do not participate in the surface film formation.
above research found by eileen
J. writes (openblooms august 06):
We did an OAT that showed the C-diff bacteria in her urine, indicating the overgrowth of the C-diff and also leaky gut. So it seems fairly certain. Are there any other tests I should do? We also did a stool analysis but that didn't identify any in her stool. It was the OAT that indicated it. Do you all know anyone who went the antibiotic route?
I know when she had an ear infection months ago, her stools normalized completely on the antibiotic, but of course went back to abnormal when antibiotic was done. Just curious as to what the pros/cons are to antibiotics for this bacteria. Also her stool analysis showed ZERO good bacteria!!
J. C. replies:
I believe that Saccharomyces Boulardii helps C-diff. Can anyone correct me or confirm? SB is a beneficial yeast strain that not only promotes the re-establishment of good flora, but it also kills the bad guys. It's very, very powerful stuff. When I tried it one cap gave me die off for 3 days (lots of gas, horrible head ache in the evening, bowel problems) so anyone who is going to try it be very careful. At the time it was way to strong for my son and I didn't know do go so slow.
I've been giving him Saccharomyces Cerevisiae for 2 weeks now (off and on to go slow). The adjustment was a bit difficult, rigid "I need to do this first before that" behaviors as well as melt downs came back, but he can handle a full cap now. The benefits have been amazing. He has gained 1/2 pound in the last 2 weeks and now is finally heavier than he was May 05 pre Mono. He has been asking for snacks and telling me when he's hungry for the first time in his life. One time it was 1:30am but that didn't bother me a bit. He is now eating bananas whole vs. pureed for the first time ever. He had sensory issues and would gag and wretch with little bites that I fed him. Plus he is all of a sudden eating green beans with apparently no allergic reaction and of course it is a completely new food and texture.
I must say that I have added a lot in the last few weeks, but these two yeast strands have proven to be every powerful in this house. I went a little off topic, but thought I'd spread the word. I would strongly advise against antibotics since there is so much else out there.
My DAN! suggested S. Boulardii to help combat my son's yeast and bacteria problem. The science behind it seems good, but I read somewhere that they are unsure of the side affects of immuno compromised individuals, and people with gut permiability, since it is a fungus. this freaked me out and I stopped the trial, ( which did seem to cause a die off ). My son is ASD 22 mos, SCD day 3, any experience with S. Boulardii???
I recently started my daughter on saccaromyces boulardii for yeast and her echolalia has been really bad!
Can this mean yeast die off or bad bacteria?
I use s. cerevisae and find good benefit from it, I find if I don't use it for a little while, when I start up again I will get fairly bad die off, it definitely keeps something in check for me
S. cerevisiae is the standard bread/ale yeast. I have major issues with it since it colonizes my gut and makes me very gassy. Boulardii is supposedly non-colonizing, but I haven't gotten up the guts to try it yet. :)
from a biofilm perspective, yeast, bacteria and viruses swap genes so (horizontal gene transfer) its really hard to control what is happening with taking Saccharomyces boulardii
what happens with ibs and colitis is that you get high virulence genes in the biofilm mix that create intractable conditions that can be managed at best
the biofilm carbohydrate diet offers principles that improve mangeability compared to scd
"Our results demonstrate that small differences in the carbohydrates on cell surfaces can be used to obtain specific immune reagents."
on a new anthrax antigen/antibody test article
bacteria seem to be able to cloak themselves with a carbohydrate coating.
the main mode of probiotics may not be replacement of gut flora population, but that the relatively uncloaked bacteria used in probiotics excite an immune response that can also knacker these cloaked bacteria
bacteria seem to be facile with sugars, being able to make anchoring polysaccharide strands in biofilm mode as well
you can see why scd or any diet giving permission to any sugar is going to still provide simple sugar raw material for these pathogens and the zero carb version of scd is probably the only way around this without using enzymes.
"Pathogenic bacteria commonly produce a thick, mucous-like, layer of polysaccharide. This "capsule" cloaks antigenic proteins on the bacterial surface that would otherwise provoke an immune response and thereby lead to the destruction of the bacteria. Capsular polysaccharides are water soluble, commonly acidic, and have molecular weights on the order of 100-1000 kDa. They are linear and consist of regularly repeating subunits of one ~ six monosaccharides. There is enormous structural diversity; nearly two hundred different polysaccharides are produced by E. coli alone. Mixtures of capsular polysaccharides, either conjugated or native are used as vaccines"
When the direct binding of peptidoglycan (a carbohydrate from intestinal bacteria) derived molecules to a specific protein in candida albicans takes place, it triggers interactions and "sensing" processes that induce the fungus to start growing long, threadlike tubes called hyphae, hence signifying its conversion to the virulent, life-threatening form.
peptidoglycan's can enter the bloodstream through the intestinal wall (leaky gut?)
intestinal biofilm bacteria supplying peptidoglycan's getting into the blood may be a good explanation for systemic candida
“ C. albicans can distinguish between a healthy and an unhealthy host and alter its physiology to attack. ”
“ The ability of the fungus to sense the immune status of its host may be key to its ability to colonize harmlessly in some people but become a deadly pathogen in others ”
lipopolysaccharides create breaks in the blood brain barrier hiv study
“Clearly, HIV-infected monocytes uniquely benefit from the LPS that is present in high amounts in the blood of HIV-infected people,” says Dr. Goldstein. “So when HIV-infected monocytes are 'knocking on the door' of the BBB and starting to crack it open, the LPS facilitates their entry by making the BBB more permeable, apparently by weakening blood vessel structure.”
the increasing resistance of h.pylori to the standard triple and quadruple therapies is the same as the recent worldwide outbreaks of nail fungus
the extra resistance and virulence is not just from the bacteria but but its co-biofilm formers
helicobacter pylori mutations are much more efficient biofilm formers, it could be worth trying candex and houstonni enzymes and oreganol with h. pyloi.
this is a biofilm bacteria with more or less virulent variants that lives on the skin and hair of the pubic and possibly anal area
also in the mouth and the external urethral orifice which are both biofilm areas
interestingly circumcised males are biased to having ureaplasma overgrowth problems because its an aerobic bacteria and does better with the increased oxygen at the urethral mouth not covered in foreskin
presumably circumcision was a sexual disease preventative by changing the conditions away from suiting some of the more anaerobic oriented std's, people nowadays have no idea how chronically difficult life use to be with maybe 50% of males having syphilis from about 1500 on until early 20th century
urea plasma is strongly associated with yeast biofilm synergies
mechanical damage to the urethra and dietary factors like too much vitamin C and oxalic acid are also factors
it can get into the urethral opening and cause pain in the urethra especially with dietary and supplement vitamin c
extreme infection involves discharge from the urethral opening
washing the pubic area (also the anal area may be needed to be so washed as well) with sodium bicarbonate mixed with shampoo seems to be effective in reducing it enough that it no longer ingresses into the urethra
if you have oily head hair, sodium bicarbonate mixed with shampoo strips out the oil quite effectively and the sodium bicarbonate is anti-yeast on the skin, especially if the mixure is left in the hair for a while before washing out
ammonia as a human biochemstry issue has never made sense to me, i really think its a bacteria issue since fermentative bacteria (including some types of klebsiella and clostridium) are so good at converting nitrogen to ammonia.
the bacteria use a molybdenum and a molybdenum-iron based enzyme to do this.
Re: ammonia really being a fermentative bacteria issue in the gut
Prior to scd B. had ammonia issues, visibly smelling of ammonia, sometimes on the breath and often his urine. As his leaky gut started healing, this happened less and less. Now, there are no longer ammonia smells in the urine or breath.
From the School of Microbiology and Immunology, University of New South Wales, Sydney, Australia.
"bacteria have adapted to the ecological niche provided by gastric mucus and the ability to manufacture large amounts of the enzyme urease. This enzyme breaks down endogenous urea to form ammonia, which protects the bacterium from gastric acidity"
the lactic acid bacteria may partly consume dietary oxalate, partly displace the gut flora that make it, (especially fungi making oxalate acid), and also provide reduced toxic load from the better gut flora so the normal body pathways can process oxalates more effectively
i think biofilm is especially prevalent where you get liquid to tissue interfaces like the baldder or kidneys or gall bladder and obviously the intestine as well
Use of a probiotic to decrease enteric hyperoxaluria.
Lieske JC, Goldfarb DS, De Simone C, Regnier C.
Division of Nephrology and Hypertension, Mayo Clinic, Mayo Hyperoxaluria Center, and Mayo Complementary and Integrative Medicine Program, Rochester, Minnesota 55905, USA. Lieske.John@mayo.edu
BACKGROUND: Patients with inflammatory bowel disease have a 10- to 100-fold increased risk of nephrolithiasis, with enteric hyperoxaluria being the major risk factor for these and other patients with fat malabsorptive states. Endogenous components of the intestinal microflora can potentially limit dietary oxalate absorption. METHODS: Ten patients were studied with chronic fat malabsorption, calcium oxalate stones, and hyperoxaluria thought to be caused by jejunoileal bypass (1) and Roux-en-Y gastric bypass surgery for obesity (4), dumping syndrome secondary to gastrectomy (2), celiac sprue (1), chronic pancreatitis (1), and ulcerative colitis in remission (1). For 3 months, patients received increasing doses of a lactic acid bacteria mixture (Oxadrop), VSL Pharmaceuticals), followed by a washout month. Twenty-four-hour urine collections were performed at baseline and after each month. RESULTS: Mean urinary oxalate excretion fell by 19% after 1 month (1 dose per day, P < 0.05), and oxalate excretion remained reduced by 24% during the second month (2 doses per day, P < 0.05). During the third month on 3 doses per day oxalate excretion increased slightly, so that the mean was close to the baseline established off treatment. Urinary oxalate again fell 20% from baseline during the washout period. Calcium oxalate supersaturation was reduced while on Oxadrop, largely due to the decrease in oxalate excretion, although mean changes did not reach statistical significance. CONCLUSION: Manipulation of gastrointestinal (GI) flora can influence urinary oxalate excretion to reduce urinary supersaturation levels. These changes could have a salutary effect on stone formation rates. Further studies will be needed to establish the optimal dosing regimen.
various web quotes:
Biochemist Dr. Vadivel Ganapathy has observed that a transporter in the colon called SLC5A8 plays an important role in enabling the colon to get the last bit of good out of food before the unusable is flushed away.
The research published online as an accelerated communication in the 'Journal of Biological Chemistry' notes that good bacteria in the colon produce an enzyme that releases glucose found in plant cell walls, the leftovers of broccoli and other vegetables, fruits and cereals, which cannot be digested in the small intestine.
In the oxygen-less environment of the bacteria-packed colon, bacteria ferment this glucose to use for energy which also results in the production of short-chain fatty acids, the preferred nutrients for colon cells.
Researchers at the Medical College of Georgia have found in animal and human cells that SLC5A8 is a final piece of the model, a transporter expressed by colonic cells to absorb the just-produced, energy-packed short-chain fatty acids.
"We used to teach that bacteria produced short-chain fatty acids which are used by colonic cells but it was not known that these cells possessed an efficient active transport system to absorb these fatty acids," Dr. Vadivel Ganapathy, biochemist, said.
The finding helps explain why fruits and vegetables are good for the body and not antibiotics, which wipe out good bacteria along with bad, should only be taken when absolutely necessary.
"We do not make the enzyme to digest cellulose; bacteria make the enzyme in the colon. Therefore, you need to eat dietary fiber to provide the food for bacteria. Otherwise, they are not going to survive there. Antibiotics can wipe out good bacteria as well, leaving a void where disease-causing bacteria can grow." Dr. Ganapathy, said.
The colon's main function is to collect waste from the diet and store it until it can be eliminated.
Cancer researchers at Case Western Reserve University in Ohio reported in 2003 in the 'Proceedings of the National Academy of Sciences' that they had cloned the SLC5A8 transporter from the human colon.
Dr. Ganapathy's lab actually cloned SLC5A8 from a mouse kidney three years earlier. Since his initial attempts to identify the transport function of SLC5A8 failed, he used Northern blot to investigate the tissue expression pattern of this transporter, hoping that the expression pattern would lead him to the identity of its transport function.
bifidus digests cellulose
"Actions: Lactic Acid Bacteria produce proteins that are water soluble, flavorless, antimutagenic, noncarcinogenic and do not cause allergic reactions. Certain strains of lactic acid bacteria have shown amazing results. A recent study at the Federal Research for Nutrition found that strains of lactic acid bacteria used to ferment bile provide protective factors against DNA damage and improve nutrition while combating intestinal problems (Both L. acidophilus and Bifido bacterium yielded positive results.). Lacto bacillus acidophilus produces lactase which helps digest lactose. B. bifidum increases the colon's fermentation of cellulose. Studies conducted on lactose malabsorbers using these strains have shown improved digestion along with the elimination of intolerance symptoms such as bad breath, bloating, gas and stomach cramps. Drugs including antibiotics may kill desirable colon bacteria. Multi-probiotic supplementation can help restore and maintain healthy intestinal flora."
There is a man in Chicago who claims that man cannot digest fiber especially insoluble fiber. So he takes grains and beans and has some kind of equipment to roast the stuff and turn it into ash. Anyway, he claims a great deal of the pain in the tummy is just gas from not being able to digest fiber and that he says we should cook soluble fiber. Anyway, I know of someone who has 18 loose bm's a day and within one day, his problem cleared up.
well actually this is what pressure cooking does, reduces the insoluble fiber by hydrolysis
that man must have had had out of control bacteria and biofilm in the colon who were no doubt very suprised by a sudden reduction in insoluble fiber
he may also be iodine deficent and the transporter used in the colon
"SLC5A8 is another designation for the AIT (Apical Iodide Transporter) that transports iodide from the thyroid cell into the lumen (where the thyroid hormones are created). It is found in other places in the body (e.g., kidney and colon), but in those places it seems to transport things other than iodide."
may use iodine as a bacterial population control measure
it also uptakes short chain fatty acids from the bacterial fermentation of cellulose
surgical bypass of the upper small intestine (the duodenum and jejunum) is being proposed as a cure for diabetes
of course diabetics are so grateful to have their small intestine bypassed and not have to do the BCD
it will be biofilm travelling up the pancreatic and bile ducts and also biofilm toxins in the duodenum and jejunum promoting the factors and gene expression responsible for type 2 diabetes
you would also expect to see liver issues with type 2 diabetes
rather interesting positive feedback loop in type 2 diabetes
high blood sugar levels in combination with biofilm toxins and heavy metals impair the enzyme that switches off crtc2
crtc2 stays on and keeps the liver metabolising fat to sugar so blood sugar levels continue to escalate (in combination with insulin resistance)
“ chronically elevated blood sugar levels disable fasting switch ” study
there could also be a vicious circle with higher blood sugar levels promoting a more systemic malign bioflm ingress into the body from the digestive system and the higher inflamation from more bioflm ingress deprecating pancreatic beta cell function in turn giving rise to even higher blood sugar levels
malign biofilm composition implicated in diabetes 2
thought you all might be interested in this study on a lack of fatty acid synthase in the gut being a cause of ulcerative colitis/IBS and diabetes through permission to biofilm ingress into colon and small intestine cells!
fish oil could help !
So, Friday night I was in so much pain, I decided what the heck, might as well try the L-glutamine (jarrow powder, had bought it about 3 weeks ago, but not tried it) So saturday morning I woke up (still in pain, bout needing to eat something) mixed some in with my eggs----- voila! No pain, I went through Saturday pain free (used a bit more Saturday evening at dinner) and so far am fairly painfree today
i think there's a straightout fight between erosion of the mucosal layer in the intestine by biofilm trying to grip its way in and the generation of new mucosa by the gut to shed the biofilm off
“ One of the well-established roles of glutamine in human health is its contribution to the integrity of the intestinal mucosa. This role is partly related to the fact that glutamine is a critical nitrogen source for rapidly dividing cells, such as those that line the gastro-intestinal tract. The principal location of glutamine consumption in the body (i.e., where it is broken down to glutamate at the highest rate) is in the small intestine. During times of stress, the small intestine responds by utilizing more glutamine and by more efficiently transporting glutamine that has been ingested ”
also from that page
“ As a fuel for rapidly dividing cells, glutamine makes a contribution to the immune system, especially in the rapid production of white blood cells during an infection. ”
so extra white blood cell activity will be helping to
so without going to an entro you can pretty well say theres an issue with biofilm and possibly a parasite in the small intestine
good page on white blood cell components, neutrophils may be the most signifcant here page
the major storage site of glutamine in muscle, so maybe too much exercise is very consuming of glutamine
i wonder if thats why minna mettinen (lil ghostie to those who remember her) embarked on a program of extreme exercise in the last several years to consume glutamine which an excess of in the spinal cord is one of the causes of ALS which unfortunately she has
its really sad, the disease is progressing and i think her time is limited page
reducing glutamine may also be why she is vegan
the eggs will have been synergistic with the glutamine i think
laura, i don't think our guts are that different, if i have stomach/intestinal pain its from too much biofilm feeding on stewed apple or the like which i eat heaps of and not enough glutamine and co factor amino acids which adding gelatine to feral broths seems to give enough of
this is why i am also keen on pasturizing all the fruit possible
there is bad interaction between too much calcium and glutamine though
A few years back I tried some L-glutamine thinking I would give it to K. It didn't do anything for me but gave me a yeast flare. I did give some to K knowing how bad her gut was hoping for not a yeast flare but better gut health but her seizures kicked in full bore all the sudden. I called the company I got it from and they told me that glutamine has been known to cause seizures in some asd kids with seizure disorders. Never tried it again for myself or her. K. is highly reactive to any glutamate in foods though so maybe there is a corellation. Glad you're feeling better though.
L. writes again:
I have also never heard of glutamine worsening crohns. I took Glutamine briefly and found it helped tremendously, but I stopped taking it because I read about some of the neurotoxic properties of it and how it could cause seizures. Anyone else have any info on this?
my experience is calcium and glutamine together are very neurotoxic and you can tell that sort of neurotoxicity by feeling 'overflat'
usually if something works, i go with it until i run into problems, but the secret is to be on the look-out for problems early
in your shoes i'd be tempted to experiment a bit more with the glutamine and think about how to offset the neurotoxicity
when you are taking it, i'd really cut back on dairy
glutamine is a strong promoter of white blood cells in the gut wall which are immune cells which points to a biofilm with some high virulence genes
its basically an attempt to control blood sugar levels through food, presumably the "zone" is in fact a region of semi-normal control of blood sugar through dietary modulation
there would be underlying issues of insulin resistance, biofilm and pancreatic insufficiency that are not addressed
the ratio's business is nonsense because it treats food as a commodity and makes no allowance for quality, type differences and other variables
theoretically the zone diet is antiquated
the approach is scd/bcd ignorant and well illustrates the usual american pechant for the half understood, over-marketed
“ Anne, an old friend of mine, walked up to Barry Sears at the Tom Landry Sports Medicine and Research Center in Dallas.
She complained that the program outlined in his book, Enter The Zone -- more lean meat, egg whites, poultry and fish, while limiting many grains, vegetables, and fruits -- just didn't work for her. She didn't feel good, and her performance level (swimming) had declined. Anne was now back on her vegetables, fruits, and whole grains.
"Stay with what works best," he said, "but you know, Anne, it's not the fat and protein that's so important. It's the effect of carbohydrates upon hormones and insulin levels." ”
i had a criticism that the veg site i took this quote from was looney, my reply is as follows:
“you have yet to learn something about problem solving, the veg site is looney but you have to pick the diamond out and leave the rest
the diamond was annes convo with sears, an authentic transcript like that is hard to come by”
has to be read very slowly
i wake and feel the fell of dark, not day.
he's really autistic, even got some biofilm imagery
what hours, o what black hoürs we have spent
this night! what sights you, heart, saw; ways you went!
and more must, in yet longer light's delay.
with witness i speak this. but where i say
hours i mean years, mean life. and my lament
is cries countless, cries like dead letters sent
to dearest him that lives alas! away.
i am gall, i am heartburn. god's most deep decree
bitter would have me taste: my taste was me;
bones built in me, flesh filled, blood brimmed the curse.
selfyeast of spirit a dull dough sours. i see
the lost are like this, and their scourge to be
as i am mine, their sweating selves; but worse.
yeah, it's biofilm sculpture
can relate to the expressions
as regards enzymes and biofilm , there is something to nattokinase and most likely serrapeptase
nattokinase is not that expensive, but my personal experience is that it tends to hit good as well as bad flora, as well as causing migraine on a blood thinning/clotting rebound
but probably there is a potential sorta "candex - no fenol - candex -nattokinase - serrapeptase - peptizyde" cross enzyme design
or maybe there isn't
dr. william davis and comments on nattokinase and fibrinolyitics
“ any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. that's why all medically used fibrinolytics are given intravenously ”
boston, June, 2010 – A single species of bacteria that lives in the gut is able to trigger a cascade of immune responses that can ultimately result in the development of arthritis.
Our gut, like that of most mammals, is filled with thousands of species of bacteria, many of which are helpful and aid in the development of a normal, healthy immune system. Gut-residing bacteria can also play a role in disorders of the immune system, especially autoimmune disorders in which the body attacks its own cells.
"In the absence of all bacteria, these mice (bred to be prone to arthritis) didn't develop arthritis, but the introduction of a single bacterium was enough to jump-start the immune process that leads to development of the disease."
The researchers began by raising arthritis-prone mice in a germ-free environment. The mice had much lower levels of arthritis-causing autoantibodies than mice raised in a non-germ-free facility. The germ-free mice also showed strong attenuation in the onset and severity of clinical arthritis.
At three weeks of age, some mice were transferred to a non-germ-free facility and the researchers introduced segmented filamentous bacteria into their systems. When they introduced this normally-occurring bacteria into the mice, the animals rapidly began producing auto-antibodies and developed arthritis within four days.
these bacteria do not cause the mice to "catch" arthritis. "It's more that they have the genetic susceptibility, and this bacterium creates an environment that allows this genetic susceptibility to play out, it's an interaction between genetics and the environment."
The team mapped out the complex chain of events leading to arthritis. The segmented filamentous bacteria cause the animals to produce more of a particular subset of T cells. The immune system reacts to the activity of the T cells as if to a foreign threat and produces autoantibodies that trigger the devastating disease.
One surprising finding was that bacteria in the gut could influence the development of an autoimmune disease affecting tissues distant from the gut. Diseases such as irritable bowel syndrome have been linked to gut-residing bacteria, but this study is unique in showing the mechanism by which a bacterium in the gut can influence the development of an autoimmune response that ends in inflammation and pain in the joints.
The team will continue to use this mouse model of arthritis to answer questions about the link between the disease and autoimmune response. Next, they plan on tackling the molecular explanation of how these bacteria promote the development of this particular subset of T cells and to explore connections with other autoimmune diseases, in particular type-1 diabetes.
geothermal ligands are the chemical starting point for life
what this implies is there is other intelligent life in the universe
it's not probable, it's certain, all no doubt with their equivalent of biofilms as well
the ligands are pretty basic to functional biochemistry and the compendium and BCD supplement principles, for instance why non protein bound mineral forms suit bad bacteria so much!
the extreme necrosis you hear about is biofilm infection
so i would say people with biofilm and immune system issues can get tripped into these staph like wounds by the bites
a white tailed spider bite in a small area like that, it's probably about as severe an injury as you can get, maybe as bad as a third degree burn given the toxic chemical nature of it
interestingly you can see how white tailed spiders would have bad biofilm on their mandibles and hence potentially seed a chronic necrotizing wound, but the spider wasp sting which is unfelt when it occurs and is dangerously allergenic for some people doesn't have biofilm in the same way not being a mouthpart!
white tail spider bites give a circular red area, an inch across? with a pustular center?
35% hydrogen peroxide on the bite area helps and maybe DMSO as well, but full recovery is a matter of months !
taking MSM helps with spider wasp bites, recovery can take a week or so tho !
i do know someone who went into analeptic shock from a spider wasp bite !