Cruiser,
You've got my attention as uwe didn't have any secrets.
Wasn't that his secret? That's what I got from him.
This:::
http://www.lioncity.net/buddhism/index.php?s=e97fa035fb6a1f9c349730a1e272d318&act=Attach&type=post&id=4475
What could be better for a budding Buddhist or high strung Nihilist?
http://en.wikipedia.org/wiki/Nihilism
Your link above looks like old hash from the p forum? LOL
Are these guys that far behind us over there? <g>
Is Uwe a state of mind now?
Or is he koning (nope), nonbagger or shaman? LOL
Let me guess. Either you or manfred is shaman? <w>
http://www.psoriasis.org/forum/search.php?searchid=1551496
Ok .. i know who it is. Mum's the word.
Are we posting the same things in both groups? LOL
http://www.psoriasis.org/forum/showthread.php?p=345808#post345808
Back to the revelation of your quote:
PGE2 (the BAD GUY) has also been treated here in detail. How
come you guys don't ask?
PGE2 release from AA (where have you been cruiser? LOL)
http://en.wikipedia.org/wiki/Fever#PGE2_release
http://en.wikipedia.org/wiki/Arachidonic_acid
OMega-6 (like from soy bean oil--- duh... randall's arch
nemesis..LOL)
http://en.wikipedia.org/wiki/Omega-6_fatty_acid
Lets see n:6 or n-6 or w6 or http://en.wikipedia.org/wiki/Linoleic_acid
etc.
And that takes us back to
http://en.wikipedia.org/wiki/Desaturase
http://en.wikipedia.org/wiki/Stearoyl-CoA_desaturase-1
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?group=alt.support.skin-diseases.psoriasis&q=omega-6&qt_g=Search+this+group
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?group=alt.support.skin-diseases.psoriasis&q=w6&qt_g=Search+this+group
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?group=alt.support.skin-diseases.psoriasis&q=n6&qt_g=Search+this+group
Here's some news.
Even if you cut out all fats/lipids that could enter inflammatory
pathways, your
body can still make it itself. LOL :(
I'm pretty positive even the most severe amongst us has the greatest
capacity at this trick. So what does he do? Besides try to correct the
gene? OK.. forgot to don't believe in DNA for these things. Or do you
now?
Why don't you do Benjamin's 30 day fast? Can we get your wife to
stay away that long? LOL
If all the diets don't work, then biologicals or low dose JX cocktails
are
in order.
Heaven's to Betsy they'd try the wit kit.... :(
But one of these days, even the dullest may find the truths of
the gut and BUTT..LOL
Even these dudes: "Beyond Probiotics" haven't come to the
light yet:: Their getting so close you'd think the BURN would
wake them UP: NOPE
http://www.vrp.com/articles.aspx?ProdID=art2284&zTYPE=2
To bad they don't get the genius of the wit kit. LOL
Now it's a ______secret_____ that you'll never KNOW...<w>
Cruiser you just don't GET IT....& never will most likely.
You have to stick that thing up your yin/yang to put
the good flora back in you....
Otherwise your stuck with an emPty box I suPPose. LOL
Or worse... one full of nasty BAD flora.... <w> <g> & ;~/
randall...yeah..time for some exercise.. :)
The end of that last one didn't feel or sound right.
I mean, it could have been doctored uP some...
It didn't have any dioxin in an abstract with a new-ish inflammation
pathway....
see: (the previous one did <g>)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/5c9957e61ee3e30d
&
I was sitting here thinking, just like BJ, when HE said something
about
LL37 and pathogenesis of psoriasis in his Barney's blog.
I said to myself....
Self---
Yes---
It's the OLD BASIC helix looP helix again. Yeah that's what
I was thinking:
http://en.wikipedia.org/wiki/Basic_helix-loop-helix
http://en.wikipedia.org/wiki/Structural_motif
No, no, don't be a folded protein.. please NO.. <g>
What then?
The good old aryl hydrocarbon receptor (AhR) & the KICKer Th17?
Yes, yes... could it BE?
Sure why not:
http://en.wikipedia.org/wiki/Aryl_hydrocarbon_receptor
One more NOT very clear pathway for inflammation?
But hey. This one doesn't need any DNA for cruiser?
http://www.news-medical.net/?id=36720
Environmental factors linked to development of autoimmune diseases
Published: Sunday, 30-Mar-2008
Medical Research News
Scientists working at the MRC National Institute for Medical Research
have shown that environmental factors can influence the development of
autoimmune diseases like multiple sclerosis.
A team led by Dr Brigitta Stockinger has identified a molecular
mechanism that links a wide range of environmental factors to the
autoimmune reactions in which immune system cells attack body tissue.
The results are published online in Nature.
The research focused on a protein called the aryl hydrocarbon receptor
(AhR). Activation of the AhR causes enzymes to be produced that are
involved in reducing the toxic effect of a wide range of chemicals on
the human body. Many of these, such as dioxin, are generated in
industrial processes. The research found that stimulation of AhR by
environmental factors could be involved in development of autoimmune
disease.
The researchers looked at the effect that both AhR and environmental
factors had on autoimmune disease in mice.
Dr Stockinger said: ''Multiple factors can influence the development
of autoimmune diseases, these include genetics, hormones, diet, the
presence of infection or exposure to chemical and environmental
irritants. Autoimmune diseases are becoming increasingly common in
industrialised countries and it is likely that this is connected to
environmental factors.''
The AhR is present in a group of T helper cells called Th17 in both
the mouse and human immune systems. T helper cells generate a response
to infection by stimulating the immune cells that produce antibodies
and those that destroy other infected cells.
Under normal circumstances, Th17 cells are important in mounting an
immune reaction to fungal and bacterial infection. Th17 cell activity
is also the cause of some autoimmune diseases including multiple
sclerosis and rheumatoid arthritis.
The research found that if AhR is activated in mice while Th17 cells
are developing, the proportion of Th17 cells present in the body
increases and so the potential for the development of autoimmune
disease is enhanced. The AhR is activated by environmental factors.
Dr Stockinger explains: ''The AhR system can potentially react to an
astounding range of factors, from environmental pollutants to
particular foods or even hormone levels. So here we have identified a
molecular mechanism that shows how such a wide range of environmental
factors could be directly linked to the cells that cause autoimmune
reactions.''
In comparison, mice that lack AhR still develop Th17 cells and T
helper cell responses but they don't have enhanced numbers of these
cells. This suggests that AhR interaction with environmental factors
leads to an increase in the number of Th17 cells and may contribute to
the onset or development of autoimmune diseases in genetically
susceptible individuals. In addition, the research showed that
stimulation of AhR resulted in faster development of autoimmunity with
greater severity. This means that environmental factors are
interacting with genetic factors to generate a detrimental autoimmune
reaction.
Dr Stockinger concludes: ''The discovery that the stimulation of AhR
by environmental pollutants can accelerate the development of
autoimmune reactions and the severity of symptoms raises intriguing
possibilities and warrants closer examination of a possible role of
AhR in human autoimmune diseases."
=========================
OK...
OH WAIT..
I was reading this and then thinking something...
What was it again?
Oh?
I'm being what with decaying what on me? lol
What?
You swine...
Who me?
NO..
Who's on first?
What?
What's on second...
HUH?
try:
http://www.baseball-almanac.com/humor4.shtml
or
http://www.clown-ministry.com/index_1.php?/site/articles/whos_on_first_script_classic_baseball_routine_abbott_and_costello/
Geez, looks longer then I want to spend with it.
Just like me?
randall.... .P is on first.. U is 2nd... :)
Holy Ghost and Mother of God....
Look..
http://www.wellnessresources.com/
This was on April 1st on this site:
Tuesday, April 01, 2008
Friendly Flora Prevents Tissue Destruction
Byron Richards, CCN
An interesting study shows that friendly flora (lactic acid bacteria
or acidophilus) helps prevent the destruction of important structural
components of the digestive tract (chondroitin sulfates and hyaluronic
acid). For many years I have observed that individuals who eat too
much sugar or who have an imbalanced digestive tract have an increase
in joint pains and aches. I have seen this issue cause serious
problems, including arthritis in children.
Generally I view this problem as being caused by the toxic metabolites
of hostile bacteria or Candida Albicans, and inflammatory signals
coming directly from such organisms - a view that is confirmed by the
current study. Additionally, by replenishing friendly acidophilus the
rate at which important structural building blocks were degraded was
normalized.
This is an extremely important finding for any person with irritable
bowel, as it is now clear that the hostile organisms are actually
directly weakening and damaging the lining of the GI tract.
It is also an important finding for general joint aches and pains.
This is because an inflamed digestive tract has "first dibs" on
structural repair nutrients due to the extreme importance of the
digestive tract. This can easily cause a shortage of chondroitin
sulfates and hyaluronic acid in joints like the hip or knee.
Digestive problems have a triple negative effect on the structure of
the GI tract lining and joints everywhere:
1) Hostile organisms produce toxins that irritate tissues.
2) Hostile organisms produce inflammatory signals that further damage
tissue anywhere in the body.
3) Hostile organisms accelerate the breakdown of structurally
essential building blocks, which can easily lead to chronically
inflamed digestion as well as loss of cartilage in joints.
Friendly acidophilus can help stop this problem. Supplemental
hyaluronic acid and chondroitin sulfates can be taken to help correct
the structural deficiencies that are leading to accelerated wear and
tear.
=====================================
I'm praying that you see the light....
Go for the light...
randall.... hey! I can only try...
ps...
For those folks unable to open this link from two posts prior
on this thread::::
This is from:
Beyond Probiotics
Hidden Causes of GI Dysfunction
By Chris D. Meletis, ND
Often, in the absence of overt disease, the extent of an individual's
colon-supporting supplement regimen consists exclusively of consuming
a good probiotic. Yet, in order for the good bacteria found in
probiotics to flourish in the colonic environment, there are other
steps we need to take to ensure our gut is hospitable to the friendly
bacteria our bodies need to thrive--regardless of whether an individual
is healthy or whether that individual suffers from irritable bowel
syndrome or another gastrointestinal disease. The colon is essentially
our body's compost pile, used to nurture our garden of friendly flora.
There are two often-overlooked aspects of gut health that are
essential to keeping our colon healthy and to ensure it remains a
hospitable environment where good bacteria can thrive. First, gut
health is linked to a substance called butyrate. If the intestine
isn't working at its optimal best, levels of butyrate can undergo a
decline, putting individuals at risk for colon cancer. Butyrate levels
are closely tied to the health of the intestine and to levels of
friendly flora found in the gut.
A second aspect of gut health is known as intestinal permeability.
This can be a huge factor, even in seemingly healthy individuals.
Intestinal permeability refers to the potential for nutrients and
bacteria to escape through a weakened intestinal wall. When intestinal
permeability is increased, food and nutrient absorption is impaired.
Dysfunction in intestinal permeability can result in leaky gut
syndrome, where larger molecules in the intestines pass through into
the blood. This can trigger immediate damage and immune system
reactions since these large molecules are perceived as foreign.
Progressive damage occurs to the intestinal lining, eventually
allowing disease-causing bacteria, undigested food particles, and
toxins to pass directly into the bloodstream.
Dysfunctions in intestinal permeability are associated not only with
intestinal diseases such as ulcerative colitis, irritable bowel
syndrome and Crohn's disease, but also with chronic fatigue syndrome,
psoriasis, food allergies, autoimmune disease and arthritis. Impaired
intestinal permeability also occurs in patients undergoing
chemotherapy and in heart disease patients.
I briefly discussed intestinal permeability in my last article on GI
health. In this article, I will go into further detail about this
damaging aspect of intestinal health and explain how increasing
butyrate can be a powerful tool in not only restoring ideal colon
function but also improving energy levels and the overall health of
the body.
Building Butyrate for Colonic Health
Butyrate, a major short-chain fatty acid produced in the human gut by
bacterial fermentation of dietary fiber, exhibits strong tumor
suppressing activity. Butyrate is an important energy source for cells
lining the intestine and plays a role in the maintenance of colonic
balance. Butyrate exerts potent effects on a variety of colonic
mucosal functions such as inhibition of inflammation and
carcinogenesis. Butyrate also reinforces various components that play
a role in the colonic defense barrier and decrease oxidative stress.
In addition, butyrate may promote satiety.1
Low levels of butyrate are linked to increased risk of colon cancer. A
loss of balance in the colon caused by either genetic mutations or
environmental factors such as dietary habits can increase the risk for
the formation of aberrant crypt foci (the earliest identifiable
cancerous lesions in the colon) and ultimately the development of
colon cancer. Evidence exists that butyrate reduces the number and the
size of aberrant crypt foci in the colon.2
Butyrate's inhibition of colon cancer is thought to arise from its
ability to act as a natural histone deacetylase inhibitor, which
results in activation of certain genes known to induce apoptosis (cell
death) in cancer cells.2
Low butyrate levels occur in healthy humans prior to the onset of
disease, often in response to a poor diet high in sugar and low in
fiber. Low butyrate levels also are found in disease states such as
ulcerative colitis and Crohn's disease, especially in patients with
moderate to severe mucosal inflammation.3 The monocarboxylate
transporter helps colon cells uptake butyrate and during inflammatory
bowel disease the monocarboxylate transporter is impaired, preventing
the butyrate from getting to the cells.4
The Colonic Barrier and Overall Health
Abnormal intestinal permeability, like low butyrate levels, is another
concern that can serve as a hidden reason why we might not be feeling
our optimal best. A dysfunction can present in intestinal permeability
when an individual is consuming a less than optimal diet or due to
other factors such as psychological stress.5
Intestinal permeability, in fact, may be the main cause behind why the
body becomes sensitive to a particular type of food. One group of
researchers evaluated the intestinal permeability in subjects with
adverse reactions to food. Twenty-one subjects with a food allergy and
20 with food hypersensitivity who were on allergen-free diets were
enrolled and divided into four groups according to the seriousness of
their referred clinical symptoms. The study authors found
statistically significant differences in intestinal permeability in
subjects with food allergy or hypersensitivity compared to control
patients. The worse the intestinal permeability, the more serious the
clinical symptoms in patients with food allergy and hypersensitivity.6
According to the researchers, "The present data demonstrate that
impaired intestinal permeability, measured in our conditions, is
present in all subjects with adverse reactions to food. In addition,
for the first time, we report a statistically significant association
between the severity of referred clinical symptoms and the increasing
of Intestinal Permeability Index. These data reveal that intestinal
permeability is not strictly dependent on IgE-mediated processes but
could better be related to other mechanisms involved in early food
sensitization, as breast-feeding, or microbial environment that
influence the development of oral tolerance in early infancy."
Impaired intestinal permeability is often linked with GI diseases such
as ulcerative colitis and Crohn's. However, new research is unearthing
a surprising link between malfunctions in the colonic barrier and a
number of non-gastrointestinal conditions such as heart disease.
In a recent study, scientists evaluated the function of the gut in 22
patients with chronic heart failure (CHF) and 22 control subjects.
Chronic heart failure patients, compared with control patients, had a
35 percent increase of small intestinal permeability and a 210 percent
increase of large intestinal permeability. Additionally, higher
concentrations of adherent bacteria were found within mucus of CHF
patients compared to control subjects.7
The researchers determined, "Chronic heart failure is a multisystem
disorder in which intestinal morphology, permeability, and absorption
are modified. Increased intestinal permeability and an augmented
bacterial biofilm may contribute to the origin of both chronic
inflammation and malnutrition."
Strengthening the Colon
Raising butyrate levels and reducing the permeability of the
intestinal barrier can have far reaching consequences for our health
that extend beyond the gastrointestinal tract. Consequently,
nutritional support is key.
Increasing fiber intake through consumption of a fiber supplement is
one of the easiest ways to increase butyrate levels in the body. Fiber
is well known for its ability to protect against colon cancer and its
ability to raise butyrate levels is thought to be one of the main ways
in which it protects the colon. The benefits of dietary fiber on
inflammatory bowel disease may also be related to the production of
butyrate that occurs when fiber is fermented in the colon. Butyrate
appears to decrease the inflammatory response.8
Combining fiber and a good probiotic with specific botanicals, amino
acids and fatty acids known to reduce intestinal permeability can
provide additional support for the colon. Phosphatidylcholine, for
example, can enhance butyrate's ability to inhibit colon cancer cells,
and therefore works well with fiber to strengthen the intestinal
environment.9
The amino acid glutamine is one of the most powerful tools for
reducing intestinal permeability, thereby protecting the body against
the negative consequences of a leaky gut. In a recent review,
researchers studied the medical literature to determine if glutamine
was effective in reducing intestinal permeability in critically ill
patients. In this group of patients, intestinal permeability can have
particularly lethal consequences, causing bacteremia, sepsis, and
multiple organ failure syndrome. After studying the medical
literature, the scientists concluded that glutamine administration by
the intravenous or oral route has a protective effect that prevents or
reduces the intensity of the increase in intestinal permeability.
Glutamine also reduces the frequency of systemic infections.10
Another group of researchers drew a similar conclusion after studying
chemotherapy patients with gastrointestinal cancer. In this group of
subjects, oral glutamine decreased intestinal permeability and
maintained the intestinal barrier.11
Berberine is another substance that can help reduce intestinal
permeability and stop beneficial nutrients from escaping through the
intestinal wall.12 Berberine also is highly effective at inhibiting
the growth of pathogens that invade the colon.
In my clinical practice, I have found that the best way to improve
butyrate levels and reduce intestinal permeability is to combine a
good fiber supplement with a supplement that contains
phosphatidylcholine, L-glutamine, berberine, deglycyrrhizinated
licorice (DGL), N-acetyl glucosamine, marshmallow (Althaea
officinalis) root, cabbage powder, slippery elm (Ulmus rubra) bark,
and gamma oryzanol. This often results in an increased level of
friendly flora in the gut and maximizes the effectiveness of any
probiotic supplement consumed. After undertaking this approach,
patients often report improvement in their gastrointestinal tract and
increased overall health and energy.
Conclusion
The gut uses a disproportionate amount of energy (about 25 percent of
total oxygen consumption) for the size of the tissue (about 6 percent
of body weight).13 Consequently, it's especially important to provide
this part of the body with as much support as possible. Fiber,
probiotics, the amino acid L-glutamine, the fatty acid
phosphatidylcholine, N-acetyl glucosamine, deglycyrrhizinated licorice
and select botanicals such as marshmallow, berberine, cabbage powder
and slippery elm can help raise levels of butyrate and reduce
intestinal permeability. This approach can result in a healthier
colon, improved energy and enhanced overall health.
==============================
one small caveat:
If you like me. Or your psoriasis is like mine, then avoid the L-
glutamine
It made me flare uP...
randall.... another sign off.... cool...
>http://www.psoriasis.org/forum/showthread.php?p=350060#post350060
What the EFA chart?
He didn't even show the most interesting part, the cox pathways down
from AA.
J.
> You've got my attention as uwe didn't have any secrets.
> Wasn't that his secret? That's what I got from him.
I know that's what YOU thought.
You got from him, what you wanted to get from him. You dismissed him
from the get go because he wanted money. I guess for YOU that means he
can't have anything worthwhile to offer. That is very strange logic.
In fact it is not logic at all. It is sour grapes. You would not
gamble the time and money to find out, so you dismiss it out of hand.
I got from him, many places to find new information and a new way of
looking at the problem, and how it relates to other diseases. I doubt
I will ever find what Uwe found, but I have found a great deal
already, in the way of understanding, and I am in a much better
position to eventually find something, than I was before Uwe came
along.
I think YOU just don't get it.
I don't really think this Koning is Uwe, but he is from the same part
of the world. I think Uwe is from Demark and this guy is from the
Netherlands. Made me think of Uwe, and
I just wanted to get your attendtion.
You missed the whole point.
Yes I am posting under the name of Shaman. Cruiser was already taken
in that group.
In any case it is the Shaman post in response to Koning, that I wanted
you to see.
I wanted you to see the bit about how to make PGE-1.
Look at this:
http://www.patentstorm.us/patents/5059622-description.html
Method for reducing blood pressure levels in hypertensive persons
The present invention relates to both food products and pharmaceutical
compositions containing specified activated Omega 6 essential fatty
acids, gamma linolenic acid (GLA) and/or dihomo gamma linolenic acid
(DGLA) combined with eicosapentaenoic acid (EPA), for the modulation
of prostaglandin levels in mammals. Certain ratios of activated Omega
6 essential fatty acids and EPA successfully modulate the levels of
beneficial prostaglandins that can provide effective treatment for
existing disease states, or can be used as a prophylactic approach to
prevent the onset of disease states such as cardiovascular disease and
immune disorders. On the other hand, other ratios of the same fatty
acids have a deleterious effect on existing disease conditions by
increasing the levels of detrimental prostaglandins, and would be
considered counterproductive in the treatment or prevention of disease
states.
curiser
J
Check out the Shaman response to Koning. That's what I wanted you to
see.
Koning posted a ton of stuff, but the real interesting bit was the,
method for boosting endogenus PGE-1.
PGE-1 is a vasodilator that activates the PGE-1/PGI2 vasodilation
pathway.
Guess what if found after posting my specualtion that vasodilaiton is
involved and how that would clear psoriasis...
http://www.patentstorm.us/patents/5...escription.html
Method for reducing blood pressure levels in hypertensive persons
The present invention relates to both food products and pharmaceutical
compositions containing specified activated Omega 6 essential fatty
acids, gamma linolenic acid (GLA) and/or dihomo gamma linolenic acid
(DGLA) combined with eicosapentaenoic acid (EPA), for the modulation
of prostaglandin levels in mammals. Certain ratios of activated Omega
6 essential fatty acids and EPA successfully modulate the levels of
beneficial prostaglandins that can provide effective treatment for
existing disease states, or can be used as a prophylactic approach to
prevent the onset of disease states such as cardiovascular disease and
immune disorders. On the other hand, other ratios of the same fatty
acids have a deleterious effect on existing disease conditions by
increasing the levels of detrimental prostaglandins, and would be
considered counterproductive in the treatment or prevention of disease
states.
---------------------------------------------------
If you read the Shaman post in response to Koning, I explain in
progressive steps why I think this may work. This was before I found
the patent, which I just added by edit function.
If PGE-1 levels can be increased, this may activate PGE-1 mediated
vasorelaxation. If this can be accomplished, then this should increase
blood flow to oxygen starved psoriatic cells, which exist in a hypoxic
environment. Increased oxygen supply will boost oxygen dependent ATP
production, which is impaired under hypoxic conditions. Increased
intracellular ATP will improve the function of inhibited ATP dependent
L-Type voltage gated calcium channels, improving the influx of calcium
into psoriatic keratinocytes, which are known to be calcium deficient.
---------------------------------
I posted this previously.
http://www.nature.com/jid/journal/v114/n4/abs/5600666a.html
Intracellular calcium plays an important part in the regulation of
proliferation and differentiation of keratinocytes.
(Snip)
The mean increase in intracellular calcium of psoriatic keratinocytes
was significantly reduced compared with control keratinocytes
(Snip)
Adding adenosine triphosphate to culture medium resulted in a more
pronounced intracellular calcium increase than thapsigargin in
psoriatic keratinocytes
adenosine triphosphate = ATP
http://en.wikipedia.org/wiki/Cellular_respiration
Fuel molecules commonly used by cells in respiration include glucose,
amino acids and fatty acids, and a common oxidizing agent (electron
acceptor) is molecular oxygen (O2).
(snip)
The energy released in respiration is used to synthesize molecules
that act as a chemical storage of this energy. One of the most widely
used compounds in a cell is adenosine triphosphate (ATP) and its
stored chemical energy can be used for many processes requiring
energy, including biosynthesis,
###########################
locomotion or transportation of molecules across cell membranes.
###########################
http://www.nature.com/jid/journal/v114/n4/full/5600666a.html
Disruption of cytoskeletal microfilaments with cytochalasin D have
been shown to inhibit capacitative calcium entry in vascular
endothelial cells (Holda & Blatter 1997). This agent, however, did not
affect basal [Ca2+]i or ATP-induced increases in [Ca2+]i, which bears
homology with our results, because ATP, which is a an IP3-mediated
Ca2+-mobilizing agonist, induced a clear increase of [Ca2+]i in
psoriatic keratinocytes, whereas thapsigargin-treated psoriatic
keratinocytes only gave a fair response compared with control cells.
Certain drugs, including lithium, antimalarials, beta adrenergic
blockers,
######################
calcium channel blockers,
######################
angiotensin-converting enzyme inhibitors, and interferons,
######################
have been reported to induce psoriasis or aggravate preexisting
disease in some patients.
######################
That is the really interesting stuff to me.
Cruiser