| randall 2005-04-19, 10:37 am |
| Hi elgoog,
Thanks for this endorsement:
Those are the things to avoid. Here are the things to seek out.
Probiotics - very important, healthy gut flora - these include yogurt
with l.acidophulus, whole whey and probiotic shakes.
Lets elucidate some!
http://50connect.co.uk/50c/articlep...ating&aID=12312
We've read about their health benefits and seen those television
adverts which state that drinking a probiotic yogurt every day for a
fortnight will make you feel healthier, (or your money back!), but new
research suggests that this is not necessarily the case.
The science behind this health argument is that the addition of the
so-called 'friendly' bacteria in probiotic products, help out-number
the bad bacteria in the gut, and in doing so have a beneficial effect
on health. This belief came about because research showed that when
these bacteria are cultured with intestinal epithelial cells (the cells
that make up your gut lining), unlike other bacterial or bacterial
products, they induce an anti-inflammatory reaction. This is why it is
suggested that they are beneficial in gut conditions such as
inflammatory bowel disease (IBD), or for lesser conditions, including
that 'bloated' feeling.
However, many scientists have questioned whether the frienndly bacteria
in probotic products would actually survive the digestive process and
make it into the gut to actually do this. What's more, there are 10 to
the power 14 bacteria (that's 1000,000,000,000,000 bacteria or a
million billion bacteria), so the thousand or so in one probiotic drink
isn't going to do much. These friendly bacteria are also unable to
replicate themselves in the gut to colonise it, and outnumber the bad
bacteria, and because they can't colonise it, they can be easily
flushed out of the gut.
Research carried out by scientists at the university of Reading and
King's college London, and published by the Food Standards Agency (FSA)
set to find out whether bacteria from probiotic products survive the
digestive system.
The study was designed to find out if these bacteria survive or break
down as they pass through the digestive system, not if probiotic
products have an effect on health.
Findings suggest that not all strains of bacteria used in probiotic
products survive through the entire digeesiv system, although at least
one strain in each of the products tested survived beyond the stomach.
The research does not show if or where probiotics might have an effect.
Professor Glenn Gibson, of the School of Food Biosciences, used
laboratory models of the human gut to imitate the conditions of the
stomach, upper intestine and lower intestine. Probiotic bacteria found
in 11 different probiotic products were tested. Products included dairy
and fruit juice containing live bacteria and dry preparations in the
form of tablets, capsules and powder. All bacteria used were grown and
their numbers standardised before each experiment began.
The researchers used a model to simulate the effect adding probiotic
bacteria would have on the total number of bacteria in a typical human
digestive system. Overall, adding bacteria from probiotics did not
change the total number of bacteria in the gut.
So don't go wasting too much money on probiotic products because it
isn't likely they do all they state they can.
*******What have i said? **** You want to change the ratio of good to
bad!****
How many times have i said that good gut flora has to be implanted?
Otherwise
it won't colonize and you'll get zero help from the oral route? The
only way to get
significant results from IL-10 produced by a huge colony of good gut
flora is,
www.thewholewhey.com (a tube up the butt and a bland diet for over a
month) then your
psoriasis no matter how severe simply melts away. Trust me I know!!!
OK you say! But why?
http://news.bbc.co.uk/1/hi/health/4358285.stm
How gut bacteria escape detection
Bacteria living in the human intestine escape detection by the immune
system by disguising themselves as gut cells, researchers say.
A US team examined bacteria from the genus Bacteroides - the most
commonly found bacteria in the human gut.
They found the bacteria wrap themselves in a sugar substance derived
from molecules taken from the surface of cells in the gut.
(me now: LPS is lipid A- bad stuff- wraPPed in a sugar coating. Aren't
those bacteria clever! No! They've just been around longer and
developed commensally with us. A good garden of gut flora will
clear you, pure and simple the mother nature way. Or is that whey!)
Details of the Harvard Medical School research are in the journal
Science.
It is extremely important that the resident bacteria in our intestine
do not generate a deleterious immune response
Dr Laurie Comstock
This form of molecular mimicry may help to explain how humans tolerate
the presence of billions of bacteria in the gut without launching an
immune system attack.
The Harvard team found that Bacteroides bacteria coat themselves with a
form of fucose, a molecule which is abundant on the surface of
intestinal epithelial cells.
(I'll run some fucose abstracts I find helpful later in this post.)
Previous research has shown that Bacteroides can stimulate intestinal
epithelial cells to produce molecules such as fucose.
It now seems that the bacteria are then able to incorporate this
molecule in a slightly modified form directly into their own cells.
Digestive role
Bacteroides play a crucial role in the digestive process, helping to
break down food products and supplying some vitamins and other
nutrients that we cannot make ourselves.
Researcher Dr Laurie Comstock told the BBC News website: "Compared to
the wealth of knowledge regarding mechanisms used by bacterial
pathogens to cause disease, relatively little is known about how the
trillions of bacteria in the mammalian intestine establish and maintain
beneficial relationships with the host.
"It is extremely important that the resident bacteria in our intestine
do not generate a deleterious immune response.
"Bacteroides are able to degrade a great variety of plant
polysaccharides so that the host is able to use them for energy.
"Many of these plant polysaccharides could not be used by the host
without the aid of the bacteria."
Dr Alastair Forbes, a consultant gastroenterologist at St Mark's
Hospital, London, said the findings were interesting.
He said it was possible they could be used in the long-term to develop
new forms of probiotic treatment for gastrointestinal disorders.
Probiotics, preparations containing beneficial bacteria, have already
been used to treat conditions such as ulcerative colitis and pouchitis.
"The use of probiotics has had some success, but their use is made
difficult by the fact that the bugs tend not to persist in the gut, and
treatments have to be given week after week," Dr Forbes said.
"If there was some way of modifying bacteria so they could continue to
infect the gut, but remain safe, that would be useful."
Dr Forbes said scientists were also working on prebiotic treatments,
which provide nutrients to encourage the growth of certain bacteria.
However, he said knowledge about the bacteria which live in the gut was
still relatively limited.
It is estimated that only about 20-30% of the bacteria that inhibit the
gut have been identified.
(But, that isn't a problem if good gut flora dominates the total
ratio.)
^^^^^^^^^
Look! There is a war in our guts between pro and anti inflammatory's
gut bacteria.
If you want IL-10 to win and lower the TNF-alphas et al's then you have
to uPregulate the good flora.
Lower LPS levels will do that. I know!
Lipopolysaccharide and Gram-positive Bacteria Induced Cellular
Inflammatory Responses: Role of Heterotrimeric G{alpha}i Proteins.
Fan H, Zingarelli B, Peck OM, Teti G, Tempel GE, Halushka PV, Cook JA.
Physiology and Neuroscience, Medical university of South Carolina,
Charleston, SC, USA.
Heterotrimeric Gi proteins may play a role in lipopolysaccharide (LPS)
activated signaling through Toll-like receptor 4 (TLR4) leading to
inflammatory mediator production. Although LPS is a TLR4 ligand, the
gram-positive bacteria Staphylococcus aureus (SA) is a TLR2 ligand, and
Group B Streptococci (GBS) is neither a TLR2 nor TLR4 ligand but is
MyD88 dependent. We hypothesized that genetic deletion of Gi proteins
would alter mediator production induced by LPS and gram-positive
bacterial stimulation. We examined genetic deletion of Galphai2 or
Galphai1/3 protein in Galphai2(-/-) or Galphai1/3(-/-) knockout mice.
LPS- and heat killed SA- or GBS- induced mediator production in
splenocytes or peritoneal macrophages (M[[Oslash]];) was investigated.
There were significant increases in LPS-, SA- and GBS-induced
production of TNFalpha, and IFNgamma in splenocytes from Galphai2(-/-)
mice compared with wild type (WT) mice. Also LPS induced TNFalpha was
increased in splenocytes from Galphai1/3(-/-) mice. In contrast to
splenocytes, LPS-, SA- and GBS-induced TNFalpha, IL-10, and TxB2
productionin were decreased in M[[Oslash]]; harvested from
Galphai2(-/-) mice. Also LPS- induced production of IL-10 and TxB2 was
decreased in M[[Oslash]]; from Galphai1/3(-/-) mice. In subsequent in
vivo studies, TNFalpha levels following LPS challenge were
significantly greater in Galphai2(-/-) mice than WT mice. Also
myeloperoxidase activity, a marker of tissue neutrophil infiltration,
was significantly increased in the gut and lung from LPS treated
Galphai2(-/-) mice compared to WT mice. These data suggest that Gi
proteins differentially regulate murine TLR mediated inflammatory
cytokine production in a cell specific manner in response to both LPS
and gram-positive microbial stimuli.
PMID: 15788486
While it looks backwards,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15710900
Its not. Two pounds (One killo) of good gut flora melts psoriasis and
needs to be studied.
I can look for trials that explain it all day long. But this area like
our psoriatic skin isn't clear yet.
The anatomy of mucosal immune responses.
Garside P, Millington O, Smith KM.
Division of Immunology, Infection and Inflammation, university of
Glasgow, Glasgow, G11 6NT, United Kingdom. p.garside@clinmed.gla.ac.uk
It remains unclear how and where unresponsiveness to fed antigens is
induced. This "oral tolerance" is probably necessary to prevent the
array of immune effector mechanisms required to counteract pathogens of
the mucosae from being misdirected against food antigens or commensal
flora. It will obviously be important to dissect where, when, and how
such immunological homeostasis is maintained in the gut, but it will
also be necessary to determine whether similar inductive and effector
mechanisms are required for the therapeutic applications of oral
tolerance systemically. This may be influenced by anatomical and
microenvironmental effects on the phenotype and/or activation state of
the antigen-presenting cell (APC), which presents orally delivered
antigen. Fed antigen passes from the intestinal lumen either via the
villus epithelium and M cells in the Peyer's patches (PP) or the
mucosal lamina propria to the organized lymphoid tissues of the PP and
mesenteric lymph nodes (MLN). In addition, there is evidence that
mucosally administered antigen also gains access directly to peripheral
lymphoid organs. Each of these sites contains distinctive populations
of APCs and has unique local microenvironments that may influence the
immune response in different ways. We propose that feeding antigen in
high doses may induce clonal anergy, deletion, or altered
differentiation because it gains direct access to resting APCs in the T
cell areas of both the gut-associated lymphoid tissues (GALT) and
peripheral lymphoid organs, with presentation occurring in the absence
of productive costimulation. By contrast, low doses of tolerizing
antigen may be taken up and presented preferentially by APCs in the
GALT, where the local environment may favor the induction of regulatory
T cells. This is consistent with our own and others findings, using
adoptive transfer of TcR tg T cells. These studies have shown that
antigen-specific CD4(+) T cells are activated simultaneously in all
peripheral and gut-associated lymphoid organs after feeding high doses
of proteins, but that this may be more restricted to local tissues when
lower doses are used. Another level of anatomical control is imposed
within lymphoid organs, where migration of T cells through distinct
anatomical compartments can affect their differentiation. We find that,
in contrast to orally primed T cells, orally tolerized T cells are
unable to migrate into B cell follicles during their initial exposure
to antigen. This affects their differentiation as upon subsequent
challenge with antigen in adjuvant, tolerized T cells can be found in
follicles but are unable to provide the B cell help that primed T cells
can deliver. We hypothesize that the initial defective migration of
tolerized T cells prevents them from receiving signals from
antigen-specific B cells in follicles and results in abortive
differentiation. Thus, both gross and fine anatomical location of fed
antigen presentation may be important in mucosal immunoregulation.
PMID: 15681738
The sun vitamin (D3) and where it don't shine, galt/Th1 factors,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=15008969
randall... proflora whey works in a re-colonized good flora RATIO.
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