Report after 1 week Boron supplement
Cruiser
Greetings,
I have been supplementing Boron in the form of Borax, for one week. Here are
the results.
After eight days of supplementing Boron, and many other things with it, I
can report that I have observed a disappearance of all the little aches and
pains, at the sites of old joint injuries, that normally plaque me on a
daily basis. That is quite nice. However, I have seen not improvement in
psoriasis, either due to Boron or any other thing I am taking.
I find that my skin has a bit more glow, and my nails are shinier, which may
be related to any number of the supplements that I am using, including the
DHEA, DHA, GLA, glutathione, NAC (w/molybdenum, selenium), very high dose
ascorbic acid.
Boron regimen used:
for first 4 days 250mg/day taken in single dose at about 7-8PM.
for next 4 days 125mg/day taken in single dose at about 7-8PM
I have decided to continue supplementing with Boron at a reduced level,
switching to 30mg twice daily. There are too many health benefits from boron
for me to stop supplemeting. North Americans do not get enough Boron due to
depleted soils and poor diet.
Once the DHEA, DHA, GLA, glutathione, and NAC are used up, I will
discontinue supplementation with those. I will stop high dose Vitamin C
after another week or two. I will then be better able to assess if the
observed skin glow and nail shine are related to boron intake. I will also
continue to assess joint pain and continue to monitor for any psoriasis
changes.
I would caution, that I have only been on B12 (methylcobalamin) and Folic
acid supplements for two days. This is not long enough to make any
reasonable accessment.
Currently, I am skeptical that folic acid is of any value to me. Folic acid
in itself is not usable. It must undergo four chemical processes to be
converted to methylfolate, which the my body can use. It is unclear to me
that folic acid can be expected to reliably undergo those steps. It is known
that some people cannot make the conversion. Consequently, I am trying to
source some Natural Sources metafolin (methylfolate made by Merck), or see
if I can get my local supplement store to buy a bulk amount from Merck,
directly.
At Randall's request, I am now adding an IP6/inositol mix to my supplements.
He suggests that this is working well for him and would like to see how it
works for me. IP6 has been shown to helpful in slowing or arresting
uncontrolled cell growth in some cancers. Since psoriais manifests
uncontrolled cell growth, and since Randall is reporting good results, this
seems like a good idea.
This may potentially cloud the results of my current regimen, making even it
more difficult to determine what may be responsible for any postive result.
However, I have already decided to take a blanket approach to ascertain if
dietary supplements can clear psoriasis. That is the only result that I am
looking to ascertain at this time. If I get results, then I can later be
concerned about what worked, and what was not a factor.
Cruiser
Pete
> Currently, I am skeptical that folic acid is of any value to me.
> Folic acid in itself is not usable. It must undergo four chemical
> processes to be converted to methylfolate, which the my body can use.
> It is unclear to me that folic acid can be expected to reliably
> undergo those steps. It is known that some people cannot make the
> conversion. Consequently, I am trying to source some Natural Sources
> metafolin (methylfolate made by Merck), or see if I can get my local
> supplement store to buy a bulk amount from Merck, directly.
I came across this snippet:
http://www.findarticles.com/p/articles/mi_m0ISW/is_2003_May/ai_100767845
High-dose folic acid for psoriasis - Literature Review & Commentary -
Brief Article
Townsend Letter for Doctors and Patients, May, 2003 by Alan R. Gaby
Seven patients with long-standing psoriasis were given 20 mg of folic
acid 4 times per day. Marked improvements were noted after 3-6 months of
treatment. Three additional patients who had previously received
methotrexate treatment for psoriasis were also given folic acid. In one
patient, new lesions appeared all over the trunk in places where they
had never existed. One patient showed decided worsening and the third
patient improved considerably.
Comment: The rationale for using high-dose folic acid is based on the
fact that allopurinol, a xanthine oxidase inhibitor, is effective
against psoriasis. The author of the present study has found that folio
acid fortified with specific amounts of ascorbic acid (to keep it in the
reduced state as tetrahydrofolate) is also an effective xanthine oxidase
inhibitor. Although no controlled trials have been done with folic acid,
other clinicians have observed the same beneficial effect against
psoriasis that Oster reported more than a quarter-century ago.
Methotrexate interferes with folic acid metabolism and, for reasons that
are not clear, appears to cause an adverse reaction to high-dose folic
acid in some cases. However, for patients who have not previously been
treated with methotrexate, folic acid appears to be a safe and promising
therapy for chronic psoriasis. Of course, when using high-dose folic
acid, it is important to remember that it can mask the laboratory
diagnosis of pernicious anemia.
Oster KA. A cardiologist considers psoriasis. Cutis 1977;20:39-41.
> At Randall's request, I am now adding an IP6/inositol mix to my
> supplements. He suggests that this is working well for him and would
> like to see how it works for me. IP6 has been shown to helpful in
> slowing or arresting uncontrolled cell growth in some cancers. Since
> psoriais manifests uncontrolled cell growth, and since Randall is
> reporting good results, this seems like a good idea.
What do you mean by IP6/Inositol mix? Are you planning on taking both
Inositol Hexaphosphate (IP6) and Inositol
--
All the best,
Pete
------------------------------------------------
Home Page: http://users.bigpond.com/lansma
Location: 42°53'S; 147°19'E
cruiser
The only IP6 I could get is a mixture or inositol and IP6. Both stores that
I checked carried the same thing. Neither had IP6 on its own. In addition
the container does not specify the ammount fo IP6 in relation the the amount
of inositol. I was not too thrilled, but I took what I could get.
>The author of the present study has found that folio
> acid fortified with specific amounts of ascorbic acid (to keep it in the
> reduced state as tetrahydrofolate) is also an effective xanthine oxidase
> inhibitor. Although no controlled trials have been done with folic acid,
> other clinicians have observed the same beneficial effect against
> psoriasis that Oster reported more than a quarter-century ago.
Thanks for the tip, I have been taking the folic acid in the morning with
the B12. I will switch to taking it in the evening with the vitamin C. I
still doubt its effectiveness, compared to methylfolate. I have some
methylfolate on order, but I am not sure if I will get it. It has to be
ordered from the States and I do not know if it will make it across the
border. If I get it at all, it will likely take 6-8 weeks.
Cruiser
----- Original Message -----
From: "Pete" <lan...@bigpond.com>
Newsgroups: alt.support.skin-diseases.psoriasis
Sent: Friday, September 23, 2005 8:29 PM
Subject: Re: Report after 1 week Boron supplement
> Cruiser wrote:
>
> > Currently, I am skeptical that folic acid is of any value to me.
> > Folic acid in itself is not usable. It must undergo four chemical
> > processes to be converted to methylfolate, which the my body can use.
> > It is unclear to me that folic acid can be expected to reliably
> > undergo those steps. It is known that some people cannot make the
> > conversion. Consequently, I am trying to source some Natural Sources
> > metafolin (methylfolate made by Merck), or see if I can get my local
> > supplement store to buy a bulk amount from Merck, directly.
>
> > At Randall's request, I am now adding an IP6/inositol mix to my
> > supplements. He suggests that this is working well for him and would
> > like to see how it works for me. IP6 has been shown to helpful in
> > slowing or arresting uncontrolled cell growth in some cancers. Since
> > psoriais manifests uncontrolled cell growth, and since Randall is
> > reporting good results, this seems like a good idea.
>
randall
> Greetings,
>
> I have been supplementing Boron in the form of Borax, for one week. Here are
> the results.
>
> After eight days of supplementing Boron, and many other things with it, I
> can report that I have observed a disappearance of all the little aches and
> pains, at the sites of old joint injuries, that normally plaque me on a
> daily basis. That is quite nice. However, I have seen not improvement in
> psoriasis, either due to Boron or any other thing I am taking.
>
You should have started with the NAC alone. Just to see the effects.
It's so powerful that even uwe mentioned it, like 14 times.
Seeing as you trust him, sorta and all.
> I find that my skin has a bit more glow, and my nails are shinier, which may
> be related to any number of the supplements that I am using, including the
> DHEA, DHA, GLA, glutathione, NAC (w/molybdenum, selenium), very high dose
> ascorbic acid.
>
But are those nails less pitted? To early to tell?
> Boron regimen used:
>
> for first 4 days 250mg/day taken in single dose at about 7-8PM.
> for next 4 days 125mg/day taken in single dose at about 7-8PM
>
> I have decided to continue supplementing with Boron at a reduced level,
> switching to 30mg twice daily. There are too many health benefits from boron
> for me to stop supplemeting. North Americans do not get enough Boron due to
> depleted soils and poor diet.
>
> Once the DHEA, DHA, GLA, glutathione, and NAC are used up, I will
> discontinue supplementation with those. I will stop high dose Vitamin C
> after another week or two. I will then be better able to assess if the
> observed skin glow and nail shine are related to boron intake. I will also
> continue to assess joint pain and continue to monitor for any psoriasis
> changes.
>
> I would caution, that I have only been on B12 (methylcobalamin) and Folic
> acid supplements for two days. This is not long enough to make any
> reasonable accessment.
>
> Currently, I am skeptical that folic acid is of any value to me. Folic acid
> in itself is not usable. It must undergo four chemical processes to be
> converted to methylfolate, which the my body can use. It is unclear to me
> that folic acid can be expected to reliably undergo those steps. It is known
> that some people cannot make the conversion. Consequently, I am trying to
> source some Natural Sources metafolin (methylfolate made by Merck), or see
> if I can get my local supplement store to buy a bulk amount from Merck,
> directly.
The pressure taken off your liver by the nac alone should allow
for more positive effects. As to the rest of your laundry list,
i've gone much the same road to little clearing without the NAC.
>
> At Randall's request, I am now adding an IP6/inositol mix to my supplements.
I'm currently not on inositol. Just checked the homocysteine formula,
that i don't take but once or twice a week, and it's not in this one.
Yet, according to this abstract i seem to be ok,
http://www.thorne.com/altmedrev/fulltext/inositol3-6.html
Other then the P, and who knows if its a marker, none of the signs of a
shortage.
I am happy with the Jarrow IP6 formula.
Take your pick,
http://images.google.com/images?svnum=10&hl=en&lr=&q=jarrow+ip6&btnG=Search
> He suggests that this is working well for him and would like to see how it
> works for me. IP6 has been shown to helpful in slowing or arresting
> uncontrolled cell growth in some cancers. Since psoriais manifests
> uncontrolled cell growth, and since Randall is reporting good results, this
> seems like a good idea.
>
:)
Yet your P levels are so low to begin with, even a tiny clearing could
be a huge difference to someone that's 50% or more covered.
Say your 2-4% (? i'm guessing now) only does a 25% clearing.
That would mean a lot more to someone that's 75% covered. But maybe
not that much to someone whose mild to begin with.
> This may potentially cloud the results of my current regimen, making even it
> more difficult to determine what may be responsible for any postive result.
If and when we shall see.
I'm presuming you had/have complete reign in your diet in the past?
I've only had that since my current trials.
So, if diet has an effect, the non visible effects on you, may
allow you to take greater license that you may not otherwise by being
on the IP6.
If not then I'll take the time now to applaud your stern fast resolve.
I know from you prior posts that you watch the diet.
I watch it go in and previously worried about the toPical downstream
effects. But not right now.
I am getting tired of pigging out all the time.
But a trial is a trial and this one has blown my mind.
Not to mention, cleared my skin almost 100%.
> However, I have already decided to take a blanket approach to ascertain if
> dietary supplements can clear psoriasis. That is the only result that I am
> looking to ascertain at this time. If I get results, then I can later be
> concerned about what worked, and what was not a factor.
>
I would think that there is a certain amount of synergism to all
the supplements your taking. I may not go cold turkey so much as
cut back slowly and keep an awareness of how you look and feel.
Or you could cold turkey for a few days and then cut back slowly
and then cold turkey and cut back etc.
Hey! I'm off to find a freaking turkey sandwich now. :)
randall... IP6, not I pee yellow! NOw i don't see P plaques!
> Cruiser
randall
So how are your nails looking now? It's been what about a week?
> > I would caution, that I have only been on B12 (methylcobalamin) and Folic
> > acid supplements for two days. This is not long enough to make any
> > reasonable accessment.
> >
Ok, so how about now?
Ok, i'm going in reverse now. :(
Right knee, elbows and ankles plaquing back up. :(
So, i'm doubling the dose of IP6. My trial has been dictated by the
P, once again.
Most everything else is the same.
Could you look over these links cruiser?
Try to get a feel for what i'm thinking please?
http://www.jstage.jst.go.jp/article/bpb/28/4/28_764/_article
http://www.jstage.jst.go.jp/article/bpb/28/4/764/_pdf
Br J Dermatol. 2005 May;152(5):1022-5. Related Articles, Links
Study of a myo-inositol hexaphosphate-based cream to prevent dystrophic
calcinosis cutis.
Grases F, Perello J, Isern B, Prieto RM.
Laboratory of Renal Lithiasis Research and Biomineralization,
University Institute of Health Sciences Research (IUNICS), University
of Balearic Islands, 07122 Palma de Mallorca, Spain. fgra...@uib.es
BACKGROUND: Calcinosis cutis is a disorder caused by abnormal deposits
of calcium phosphate in the skin and is observed in diverse disorders.
Myo-inositol hexaphosphate (InsP(6)) is a diet-dependent molecule found
in all mammalian fluids and tissues, which exhibits an extraordinary
capacity as a crystallization inhibitor of calcium salts. OBJECTIVES:
To establish the effects of topically administered InsP(6) cream on
artificially provoked dystrophic calcifications in soft tissues.
METHODS: Fourteen male Wistar rats were randomly assigned into two
groups: control and treated groups. Rats were fed with an InsP(6)-free
or phytate diet. Plaque formation was induced by subcutaneous injection
of 0.1% KMnO(4) solution. From 4 days before plaque induction to the
end of the experiment, control rats were treated topically with a
standard cream, whereas treated rats were treated with the same cream
with 2% InsP(6) or phytate (as sodium salt). Calcification of plaques
was allowed to proceed for 10 days. InsP(6) in urine was determined.
The plaques were excised and weighed. RESULTS: It was found that when
InsP(6) was administered topically through a moisturizing cream (2%
InsP(6)-rich), the plaque size and weight were notably and
significantly reduced compared with the control group (1.6 +/- 1.1 mg
InsP(6)-treated, 26.7 +/- 3.0 mg control). The InsP(6) urinary levels
for animals treated with the InsP(6)-enriched cream were considerably
and significantly higher than those found in animals treated topically
with the cream without InsP(6) (16.96 +/- 4.32 mg L(-1)
InsP(6)-treated, 0.06 +/- 0.03 mg L(-1) control). CONCLUSIONS: This
demonstrates the important capacity of InsP(6) as a crystallization
inhibitor and also demonstrates that it is possible to propose topical
use as a new InsP(6) administration route.
PMID: 15888163
http://www.fsm.ac.fj/Medicine%20Website/HADIF%20website/12%20Anemia/12-%20Anemia.htm
Iron-deficiency anaemia
The human body has no way to excrete excess iron. The only way that
iron may be lost from the body is through the small amount that is lost
when cells are shed, and through blood loss. A male adult loses 1mg
iron daily through cells shed from the gut and skin in addition to iron
lost in sweat and urine. Menstruating women have higher overall losses,
due to the 30ml (15mg iron). or more lost monthly through menstrual
bleeding. The male adult has a mobile storage pool of iron of no more
than 1g, and most women would have less than this. Daily blood loss of
10-20ml (containing 5-10mg of iron). will result in negative iron
balance and depletion of storage iron fairly quickly.
Because of the difficulty with iron excretion, iron stores can only be
limited by ensuring that iron absorption is very inefficient. A normal
Western diet provides 15mg iron per day but only 1mg enters the
circulation. In iron deficiency the gut can increase the absorption of
iron, but the maximum that can be absorbed is 3-4mg daily (Anderson &
Powell, 1999).
In the early stages of iron deficiency there is gradual depletion of
storage iron, after which iron-deficient erythropoesis occurs. At this
stage the haemoglobin concentration, mean corpuscular volume, and MCH
may still be within the normal range. The classic features of iron
deficiency occur late, when with continuing negative iron balance,
anaemia develops and microcytic hypochromic cells appear in the
peripheral blood.
(...)
Factors which effect iron absorption
A large proportion of the Indian community are exclusive vegetarians or
eat meat extremely sparingly. This means that they do not have access
to readily-absorbed haem iron, but need to rely on poorly absorbed
inorganic iron from vegetable sources instead.
A number of substances in the diet are known to bind iron and prevent
its absorption. These include tannin from tea, tamarind, and phytates
as are found in unleavened breads. All of these are common in the
Indian diet.
Iron absorption is increased by simultaneous ingestion of Vitamin C. In
a 1956 study by Oldmeadow, iron deficiency anaemia in pregnant Indian
women in Fiji was noted to be seasonal, occurring more in July and
October, with a second peak in March. He determined that this was
related to decreased stores of Ascorbic acid in the Indian women, which
in turn was due to poor Vitamin C consumption outside the Mango season
(November/December). pineapple season (November). and guava season
(January?April). By contrast, Fijians appeared to eat Vitamin C-rich
foods all year around (Oldmeadow, 1956)
Can you see how i'm conflicted now with these obvious anomalies between
C and IP6?
I don't see any reason to double the C as the three grams twice a day
hasn't caused any problems.
I do have a spot of PsA in the right hand fingers due to the purines
in the highly carnivore diet.
By doubling down on the ip6 though, i would be simulating a lot more
grains.
And with that topical IP6 link above we could get more IP6 right into
the actual plaques.
Are you thinking now?
:)
randall
Hey!
Cruiser did you read the previous post in this thread?
Or did those abstracts get in the way. If so skiP them.
There's a sh*t load of them here as well. Forget them and
read the parts you get. There's a load of meat that you just
can't afford to miss in this post towards the bottom of the post. ;-/
Back to the last post.
The skin is used to shed iron. P must shed a sh*t load of it.
Do women have less P after their periods? Can you check the group for
that one?
Do you figure that ip6 cream right in the plaques will do more then
just eating
it? That would be IF the iron in the skin is more then just irony. Like
uwe attempting to cure us for a freaking buck, btw.
In my current trial i'm eating meat like crazy and normally i would be
shedding Psoriasis like crazy. Not now. How come i'm not the usual
major flake that
I would be by eating the way i am? Well...?
But i've started to go a little bit backwards and that means my P is
going forwards some. :(
Just a little ok.
What should i do?
I went to one gram a day of IP6 from my previous half gram a day.
In less then two days my p is headed back towards clear! :)
I haven't even tried the ip6 cream yet. What will i call it?
Cream your P away. Cream Away? Don't cream your genes?
Whoops, do cream them? NOt the UWE P cure formula?
In my quest to cure you and by default, me. And even guys like SC, who
simply doesn't get me. (That's ok. If you got everything 24/7 it would
be like an acid trip and then not much would get done.) I've gone back
to IP6 many times and each time from a refinement of previous P trials.
You've grabbed the shotgun and loaded up on boron and PC and everything
not
Pc. he he
Now, i'm faced with finding an explanation for why certain things have
done something positive or negative.
In your trial you may be on the uPward P curve and not even know it!
You haven't any idea if your p is stable. As from what you say it
isn't!
Can we stomach this puzzle? Of course we can.
In this next article we have an small molecule, taken orally to slow
down inflammation.
Funny how this goes isn't it? Finding something to eat to stop what you
eat that may cause the p skin stuff?
That's what use says isn't it? We eat something that dePletes something
that
helps the immune system? If it isn't NAC for uwe, then he doesn't have
any
other ducks in his hat to pull out. lol
As to real emPirical tests/trials and
Along my long path with P, i found i could change the ratio of n3 to n6
and clear. I could stop eating the high arachidonic foods and clear. I
could change my colon conditions and clear. And
some supplements and herbs could make a difference as well. I was great
at finding things to clear, but something i ate took me back to hell,
do not passs
clear do not colect $200. You know, it had a monopoly on me!
I ate my way in, could i eat my way out?
Here's that small molecule (SM) you eat for less inflammation.
Yet, what is it? Is sm really good for you?
******^^^^^^^^^^^^^^*********^^^^^^^^^^^^^^************^^^^^^^^^^^^^
Inflammation: Cooling the inflammatory response
Two groups have shown that PI3Kgamma inhibition disrupts leukocyte
activation and migration in chronic inflammatory disorders such as
rheumatoid arthritis and systemic lupus erythematosus.
Phosphoinositide 3-kinases (PI3Ks) are attractive therapeutic targets
in various diseases, such as autoimmune and inflammatory disorders and
cancer. However, a shortage of isoform-selective compounds has been an
obstacle to therapeutically targeting these enzymes. Two papers in
Nature Medicine support the promise of the PI3Kgamma isoform as a
viable therapeutic target.
PI3Ks are intracellular signalling enzymes that are involved in several
fundamental biological processes, such as cell survival and
proliferation, and vesicular trafficking. One of the drawbacks of
disrupting the activity of the PI3Ks is that some isoforms are
essential for these cellular processes; for example, knockouts of the
genes encoding the ubiquitously expressed PI3Kalpha and PI3Kbeta are
embryonically lethal in mice. However, targeting the PI3Kgamma and
PI3Kdelta isoforms would circumvent this problem because their
expression is restricted to the haematopoietic system. Mice lacking the
genes encoding these enzymes develop normally, although they do show
defects in adaptive immunity, including activation of T and B cells.
This suggests that PI3Kgamma and PI3Kdelta could be potential targets
for diseases caused by inappropriate inflammatory responses, such as
rheumatoid arthritis and systemic lupus erythematosus (SLE). Indeed,
PI3Kgamma is known to have a key role in mediating the activation and
migration of white blood cells (leukocyte chemotaxis), such as
macrophages and neutrophils during an immune response, and neutrophil
migration has been strongly implicated in the pathogenesis of
rheumatoid arthritis.
Using an automated in vitro lipid-kinase assay, Camps et al.
identified, and subsequently optimized, a series of small-molecule
inhibitors of PI3Kgamma. Crystallization of one of the compounds,
AS-604850, with PI3Kgamma facilitated the structure-based design of
AS-605240, which was found to have a greater inhibitory potency towards
PI3Kgamma. After demonstrating the inhibitory effects of these
compounds on several types of immune cells and chemokine ligands ex
vivo, the authors tested the efficacy of AS-605240 in two distinct
mouse models of rheumatoid arthritis. Oral administration of AS-605240
suppressed joint inflammation and damage in both models. Importantly,
treatment with AS-605240 afforded the same protective effects that were
observed in mice deficient in the gene encoding PI3Kgamma.
The effect of inhibiting PI3Kgamma-mediated inflammation in a model of
the chronic inflammatory autoimmune disease SLE using AS-605240 was
also investigated by Barber and colleagues. In MRL-lpr SLE-prone mice,
AS-605240, as well as reducing inflammation of the glomeruli of the
kidney (glomerulonephritis), which is a characteristic symptom of SLE,
extended the lifespan of the mice and caused no adverse side effects.
The successful development of an orally active inhibitor that is
selective for the PI3Kgamma isoform strengthens the hypothesis that
this enzyme represents a valid therapeutic target for disrupting
leukocyte activation and migration in chronic inflammatory disorders.
**************
I don't know about you, but this SM sounds good to me.
Am i doing SM to myself right now with IP6?
Or do i need IPsex? lol Sorry couldn't resist that one.
StoPPing the activation of T cells is what its all about,
http://stke.sciencemag.org/content/vol0/issue2001/images/data/CMP_7019/DC1/Singerng2.jpg
And what goes down in the gut doesn't show uP on the skin,
http://www.bioscience.org/2004/v9/af/1468/figures.htm
& more sPecific to us from bowcock and krueger,
http://ard.bmjjournals.com/content/vol64/suppl_2/images/large/ar31120.f2.jpeg
Something isn't normal in P skin, recall this
http://ard.bmjjournals.com/content/vol64/suppl_2/images/large/ar31120.f1.jpeg
How does one avoid activation?
It must be this PI3K stuff? Lets look.
^^^^^^^^^^^^^^***************^^^^^^^^^^^^^^^^^****************
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15970662
The Jak/Stat pathway: a novel way to regulate PI3K activity.
Abell K, Watson CJ.
Department of Pathology, University of Cambridge, Cambridge, UK.
Phosphoinositide 3-kinases (PI3Ks) have been grouped into three major
classes that have different substrate specificities. Class IA PI3Ks
consist of a catalytic and a regulatory subunit and have multiple
isoforms that arise from different subunit combinations. The role of
two of the small regulatory subunits, p55alpha and p50alpha, is poorly
understood. We have now identified a novel function for these subunits
and have shown that their expression is specifically induced in the
involuting mouse mammary gland where they are involved in the
downregulation of PI3K signalling and Akt/PKB activity. This abrogation
of survival signalling thru Akt/PKB and its downstream targets is
essential for the induction of apoptosis. The switch from lactation to
involution is associated with activation of the transcription factor
Stat3, by the cytokine LIF. Stat3 is essential for the induction of
apoptosis and, in the absence of Stat3 or LIF, expression of the
p55alpha and p50alpha subunits is abrogated. Surprisingly, Stat3 is a
direct regulator of p55alpha and p50alpha expression, as demonstrated
using ChIP assays, and therefore these subunits are not splicing
isoforms as previously thought. An important implication of our results
is that the p55alpha and p50alpha small regulatory subunits are
regulated independently of the larger p85alpha subunit, and have an
essential role in Stat3-mediated apoptosis in mammary gland.
PMID: 15970662
We have P jak/stat pathways don't we? Sure we do, don't we?
http://groups.google.com/groups?q=jak+stat+psoriasis&qt_s=Search
http://www.google.com/search?q=jak%20stat%20psoriasis&qt_s=Search&sa=N&tab=gw
Lets look at Pi3K,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9255069
http://www.biochemistry.org/meetings/programme.cfm?Meeting_No=H60
The awesome proliferation of inositol lipids and phosphates and their
functions has been one of the most high profile aspects of cell biology
since the 1980s, and it shows no sign of slowing down. There are now
seven known polyphosphoinositol lipids, all of which have defined
(often multiple) functions; indeed phosphatidylinositol
4,5-bisphosphate (PtdIns(4,5)P2) is involved in the regulation of at
least fifteen (and rising) physiological events. The inositol
phosphates are even more in number, and although the regulation of
their synthesis and their functions are less well understood, their
functions too are proliferating.
The enzymology of the synthesis and breakdown of inositides is, as
might be expected, proving to be a complex issue, involving many
isoforms regulated in complex fashion. In particular, the regulation of
the PI 3-kinase family, and the downstream consequences of their
products, is one of the most intensively investigated areas of
intracellular signalling.
This conference will be structured around groups of inositol-containing
compounds, but will inevitably cover a diverse range of cell biology,
not least because there are few areas of cell biology that do not
involve inositides.
http://www.fasebj.org/cgi/content/full/14/15/2618
Signaling pathways involving the inositol polyphosphates and the
polyphosphoinositides have become intricately linked with a number of
disease states. More recently, this has principally involved the
3-phosphorylated products of phosphoinositide 3-kinase, an enzyme that
itself shows oncogenic activity and has hence become of interest in the
design of antitumorigenic drugs. The downstream effectors of
phosphoinositide 3-kinase are involved in different aspects of cellular
signaling and cytoskeleton and trafficking events that are linked to
specific polyphosphoinositide binding properties of specific protein
domains, which themselves have emerging roles in specific disease
states. Our recent findings have demonstrated that there is a
selectivity of the intracellular effects of extracellularly applied
inositol polyphosphates in their abilities to inhibit a range of
growth-related in vivo assay conditions, and that these can themselves
be linked to the inhibition of the membrane localization of a green
fluorescent protein (GFP) -tagged PH domain. We propose that GFP
fusions of the polyphosphoinositides binding domains of specific
proteins of interest can be used in high-throughput investigations of
the therapeutic value of specific inositol polyphosphates analogs.
Inhibition of in vivo membrane targeting of these domains from proteins
involved in cell growth and tumorigenesis can thus be used in the
search for new anticancer drugs.-Berrie, C. P., Falasca, M. Patterns
within protein/polyphosphoinositide interactions provide specific
targets for therapeutic intervention.
*****************^^^^^^^^^^^^^^^******************^^^^^^^^^^^^^^^^^^^^^
Quantitative model of Ras/phosphoinositide 3-kinase signaling crosstalk
based on cooperative molecular assembly.
Kaur H, Park CS, Lewis JM, Haugh JM.
In growth factor-stimulated signal transduction, cell surface receptors
recruit phosphoinositide (PI) 3-kinases and Ras-specific guanine
nucleotide exchange factors (GEFs) to the plasma membrane, where they
produce 3'-phosphorylated PI lipids and Ras-GTP, respectively. As a
direct example of pathway networking, Ras-GTP also recruits and
activates PI 3-kinases. To refine the mechanism of Ras/PI 3-kinase
crosstalk and analyze its quantitative implications, we offer a
theoretical model describing the assembly of complexes involving
receptors, PI 3-kinase, and Ras-GTP. While the model poses the
possibility that a ternary receptor/PI 3-kinase/Ras complex forms in
two steps, it also encompasses the possibility that receptor/PI
3-kinase and Ras/PI 3-kinase interactions are competitive. In support
of this analysis, experiments with platelet-derived growth
factor-stimulated fibroblasts revealed that Ras apparently enhances the
affinity of PI 3-kinase for receptors; in the context of the model,
this suggests that a ternary complex does indeed form, with the second
step greatly enhanced through membrane localization and possibly
allosteric effects. The apparent contribution of Ras to PI 3-kinase
activation depends strongly on the quantities and binding affinities of
the interacting molecules, which vary across different cell types and
stimuli, and thus the model could be used to predict conditions under
which PI 3-kinase signaling is sensitive to interventions targeting
Ras.
PMID: 16159314
I need to explain my current trial (vitamin C, IP6 on top of a
carnivorous diet designed
to flare up my psoriasis) and whats happening not only with my lower
levels of psoriasis but
increasing PsA, (is it low CD59?)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12747280
Impaired expression of erythrocyte
glycosyl-phosphatidylinositol-anchored membrane CD59 in patients with
psoriatic arthritis. Relation to terminal complement pathway
activation.
Triolo G, Accardo-Palumbo A, Salli L, Ciccia F, Ferrante A, Tedesco L,
Salli S, Giardina E, Pappalardo A, Licata G.
Department of Internal Medicine, Rheumatology and Clinical Immunology
Unit, Division of Internal Medicine, Department of Pathology,
University of Palermo, Italy. tri...@tiscalinet.it
OBJECTIVE: Complement-mediated injury is regulated by many factors;
among these CD59 has been identified as a widely distributed
glycoprotein that inhibits membrane C5b-9 (terminal complement
component) formation. The aim of the study was to assess erythrocyte
CD59 expression in patients with psoriatic arthritis in order to
understand the role of CD59 in the pathogenesis. METHODS: Washed
erythrocytes from 50 patients with psoriatic arthritis, 8 with
cutaneous psoriasis and 24 healthy subjects were incubated with
monoclonal anti-CD59 antibody followed by a second FITC conjugated
antibody and fluorescence intensity analysed by FAC-Scan flow cytometer
to assess their CD59 membrane expression. SC5b-9 levels were measured
in the plasma by ELISA and results compared with CD59 values. Immune
complexes, complement C3 and C4 and rheumatoid factor were also
determined. RESULTS: Impaired expression of erythrocyte
membrane-anchored CD59 was found in patients with psoriatic arthritis;
the lowest levels were seen in active patients (p < 0.01). Increased
SC5b-9 was seen in the plasma of patients with active disease. An
inverse correlation was also found between plasma C5b-9 and the CD59
expression levels (r = -0.81, p < 0.001). CONCLUSION: The low CD59
expression on erythrocytes from patients with psoriatic arthritis may
be an index of a low tissue CD59 expression. This impairment could
facilitate the activation of complement pathway and increase the risk
for arthritis. Membrane attack complex formation in deficient membrane
bound CD59 may also exacerbate synovial cell injury and inflammation.
PMID: 12747280
What other P pathways is PI3K involved in?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7782932
1,25(OH)2D3-regulated human keratinocyte proliferation and
differentiation: basic studies and their clinical application.
Bikle DD.
University of California, VAMC Endocrine Research, San Francisco 94121,
USA.
Keratinocytes produce vitamin D, metabolize it to its most biologically
active form, 1,25(OH)2D, and respond to the 1,25(OH)2D they produce
with a decrease in proliferation and an increase in differentiation.
1,25(OH)2D production by keratinocytes is tightly controlled and
changes as the cells differentiate, increasing during the early stages
of differentiation and then decreasing again as terminal
differentiation ensues. The 1,25(OH)2D produced endogenously or
supplied exogenously acts in concert with calcium and products of
phosphoinositide metabolism to stimulate the transition from a
proliferating basal cell to a terminally differentiated corneocyte. The
mechanisms involved include changes in gene transcription and messenger
RNA stability. These antiproliferative, prodifferentiating actions of
1,25(OH)2D3 have led to its successful use in psoriasis, a
hyperproliferative skin disease, and may lead to its use as a
chemopreventive agent in malignancy.
PMID: 7782932
http://ard.bmjjournals.com/cgi/content/full/64/suppl_2/ii30
(...)
The consequence of loss of this RUNX1 site is unknown. However,
alterations in RUNX1 sites in other genes predispose to other
autoimmune diseases. In both cases these sites lie within introns. One
lies within an intron of the PD-1 (PDCD1) gene and predisposes to
systemic lupus erythematosus.13 The PD-1 gene codes for an
immunoreceptor that is a member of the Ig superfamily harbouring an
immunoreceptor tyrosine based inhibitory motif. Interaction of PD-1
with its ligand leads to inhibition of anti-CD3 induced T cell
activation by reducing interleukin (IL)-2 production and inhibition of
proliferation and cytokine production.
The other RUNX1 variant lies within an intron of SLC22A4 on chromosome
5q31 and predisposes to rheumatoid arthritis (RA).13,14 SLC22A4 is
specific to haematological and immunological tissues and is induced by
proinflammatory stimuli. It is highly expressed in the inflammatory
joints of mice with collagen induced arthritis, and it is proposed that
it may function as a transporter in lymphoid organs or an inflammatory
milieu.14 The RA associated variant leads to RUNX1 binding and it is
proposed that its excessive expression contributes to development of
RA.
RAPTOR lies in the region of psoriasis linkage on chromosome 17q25 that
was first detected in a large multiply affected family with
psoriasis.14,15 Some of the affected members in this family also
developed PsA at an early age. Hence it is tempting to speculate that a
regulatory variant in RAPTOR predisposes to both psoriasis and PsA.
RAPTOR binds to and regulates the function of mTOR (target of
rapamycin), a key regulator of T cell function and growth. mTOR is a
component of a cytokine triggered protein kinase cascade leading to the
phosphorylation of the eukaryotic initiation factor (eIF)-4E binding
protein, PHAS-1, in activated T lymphocytes. This event promotes G1
phase progression by stimulating eIF-4E dependent translation
initiation.15,16 Rapamycin binds to and blocks the function of mTOR,
leading to immunosuppression. <sniP>
16. Brunn GJ, Williams J, Sabers C, Wiederrecht G, Lawrence JC Jr,
Abraham RT. Direct inhibition of the signaling functions of the
mammalian target of rapamycin by the phosphoinositide 3-kinase
inhibitors, wortmannin and LY294002. EMBO J 1996;15:5256-67.
http://embojournal.npgjournals.com/cgi/content/abstract/15/19/5256?ijkey=b63ecd4496ba3cc58cd794fc3e0e502b3a1af43e&keytype2=tf_ipsecsha
**********************&&&&&&&&&&&&&&&&&&&&^^^^^^^^^^^^^^^^^^******************
Going back to 1979
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=526045
Arch Dermatol Res. 1979 Oct;266(2):177-80. s
The phospholipid pattern in the involved and the uninvolved
psoriatic epidermis.
Tsambaos D, Mahrle G.
The phospholipid pattern of the involved and the uninvolved
epidermis from 48 psoriatic patients and of the normal epidermis from
23 healthy controls was determined by thin-layer chromatography. A
higher amount of total phospholipids was found only in the involved
psoriatic epidermis, whereas significant alterations in the
phospholipid pattern were observed in the psoriatic lesion and in the
lesion-free epidermis. Namely, the decrease of phosphatidylserine and
the increase of phosphatidylinositol were identically present in both
the involved and the uninvolved psoriatic epidermis. It seems likely
that these alterations in the phospholipid pattern in psoriasis may be
related to subclinical alterations of the epidermis in this disease.
PMID: 526045
********************^^^^^^^^^^^^^^***********^^^^^^^^^^^^^^^^*******************
Then again in 1989,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2542414
Increased phosphatidylinositol kinase activity in psoriatic epidermis.
Pike MC, Lee CS, Elder JT, Voorhees JJ, Fisher GJ.
Arthritis Unit, Massachusetts General Hospital, Boston 02114.
Phosphatidylinositol (PI) kinase is activated by growth factors, such
as epidermal growth factor (EGF), and is thought to be involved in
cellular proliferation. Psoriasis is a hyperproliferative epidermal
disease in which EGF receptor expression is altered and phospholipase C
activity is increased. Considering the potential importance of growth
factor stimulated phosphoinositide metabolism in the genesis of
abnormal growth, we measured PI kinase activity in epidermal keratome
biopsies from normal skin and the lesional and nonlesional skin of
psoriatic patients. The PI kinase activity in 10 psoriatic involved
plaques was increased 6.7-fold (Vmax = 67.1 +/- 23.9 pmol formed/min/mg
protein +/- SE) when compared with 11 normal epidermal biopsies (Vmax =
10.0 +/- 1.3 pmol/min/mg protein, p less than 0.025). Similar results
were noted when enzyme activity was standardized using DNA content. The
apparent Km of PI kinase for ATP in involved psoriatic biopsies (0.45
+/- 0.14 mM) was also significantly (p less than 0.025) increased
compared with normals (0.11 +/- 0.02 mM). The PI kinase activity in 11
biopsies of nonlesional psoriatic epidermis was not statistically
different from normal epidermis. Both psoriatic and normal PI kinases
required Mg++ and were inhibited by Ca++. The polyamine, spermine, a
known activator of PI kinase in other tissues, stimulated normal but
not psoriatic epidermal PI kinase. Both normal and psoriatic PI kinase
activities had an apparent mol wt of 85,000. Increased synthesis of
phosphoinositides by PI kinase in psoriatic tissue may provide more
substrate for phospholipase C; a key enzyme in growth factor-mediated
signal transduction.
PMID: 2542414
What are these polyamines and spermine activators? Oh! This goes back
to putrescine.
http://groups.google.com/groups?q=polyamine%2C+spermine+putrescine+psoriasis&qt_s=Search
I should have done a crap in the skin thread. I did! Ok, what i mean is
i should have called it that.
What do we call this psoriasis craP?
http://broadmining.com/Putrescine
To get a feel for what putrescine is, get some raw meat and let it go
bad. You
can smell the putrescine crap. Now, in the randalls proflora theory,
one changes the terrain of his/her lower
colon till it's nearly all good sweet lacti loving bacteria (like
having 2 pounds/1 killo of yogurt ) down there.
Each time you poop, it's neatly and sweetly coated in butt yogurt. lol
Well it is. If those BM's aren't sliPPing right outa you, then you
don't have enough
good flora down there.
Ok now. Alrighy then. Back to the meat trials.
So, when you leave your raw meat out to putrify, also dip one piece of
raw meat in yogurt and leave it next to the other one. The one covered
in yogurt will take much longer to go bad.
Long enough that most people who have impaired digestion/absorption
will just pass it thru their system without this crap getting out into
their skin. I should go into an explanation of LPS now, butt won't. <g>
Even though its central to the randall theory of craP.
So, where are we? What are we is more like it. Sh*t skin people? Or
what?
Well, we know these polyamines (spermine, putrescine, etc) are
neccessary for cell growth,
http://www.pediatrie.be/POLINMIL.htm
If mother nature puts some in the milk it can't be all bad.
Yet, we need to dial down the skin growth already. Isn't P skin really
unabated cell growth?
What inhibits polyamine biosynthesis?
http://www.niaid.nih.gov/daids/dtpdb/030965.asp
Are we making this map crap endogenously to further foil the
unprocessing of P?
I don't know. But will check it out.
But why have the freaking problem of to much cell growth factors?
Either go vegetarian or change your gut to handle the meat you toss
down there.
Back to the old P abstracts,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7513354&query_hl=1
Glycosylphosphatidylinositol (GPI)-anchored membrane proteins are
constitutively down-regulated in psoriatic skin.
Venneker GT, Das PK, Meinardi MM, van Marle J, van Veen HA, Bos JD,
Asghar SS.
Department of Dermatology, University of Amsterdam, Academisch Medisch
Centrum, The Netherlands.
Hyperproliferation of keratinocytes (KCs) in psoriasis has been found
to be associated with excessive activation of a phospholipase C
(PLC)/protein kinase C (PKC) signal transduction system. The molecular
species of PLCs which are activated in psoriasis have not been
thoroughly investigated. It was envisaged that if
glycosylphosphatidylinositol (GPI)-specific PLC was activated in the
membrane of psoriatic epidermal cells, it would render these cells
devoid of those proteins which are anchored to the cell membrane
through their GPI moiety. In order to test this possibility, four GPI
proteins (CD16, CD55, CD58, and CD59) were determined
immunohistochemically in normal and psoriatic skin. In normal skin,
CD55 and CD59 were strongly expressed on epithelium and vascular
structures, whereas CD16 and CD58 were strongly expressed only on
epithelium. The expression of all four GPI proteins was decreased in
non-lesional psoriatic skin and virtually abolished in lesional
psoriatic skin. A control transmembrane protein, CD46, was strongly
expressed in normal and non-lesional psoriatic skin, and its expression
was not significantly decreased in psoriatic lesions. The absence or
reduction of GPI proteins was not seen in the lesions of several other
inflammatory and proliferative diseases studied.
PMID: 7513354
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2170539
What happened over the years? They had there fingers on this thing and
along the way they went to their pharmacist drug making couterparts and
realized that to make something that would actually block the crap in
the colon, it
would cut them out of the business of making money with a drug?
It now figures we have biological drugs that cost a freaking mint
($10-30,000 per year) and don't actually cure you!!!
How logical are BIOlogicals? Business wise, very logical for them. Not
very for us!
Is it not incumbent for you to clear you?
If you want long lasting relief it seems so.
I'll stick with my IP6 and vitamin C. I've added one more twist now.
The PePPermint twist,
http://www.manfredwirth.de/dee14.jpg
randall... well, i can still dance to that tune.
randall
Did you give uP or is your P surging forward? Or I'm hoPing your on a
tropical cruise.
And not with computation powers. :(
As the weather turns I know my P usually kicks uP some flakes.
Time to hoover?
Ok i've not given uP. According to Irvcomm and Winston, never give uP,
ever.
Churchill being somewhat more famous outside the P group,
http://www.school-for-champions.com/speeches/churchill_nevergiveup.htm
What iv'e put forward in the last three posts is in this never give uP
attitude.
My current IP6/Ascorbic acid (vitamin C) trial screams for recognition.
All psoriatics that could/may use this cheap therapy can benefit.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15040469
In vivo assessment of iron and ascorbic acid in psoriatic dermis.
Leveque N, Robin S, Muret P, Mac-Mary S, Makki S, Berthelot A, Kantelip
JP, Humbert P.
Laboratory of Cutaneous Bioengineering, Faculty of Medicine and
Pharmacy, Besancon, France.
Reactive oxygen species play an important role in inflammatory skin
diseases such as psoriasis. Reactive oxygen species synthesis is
catalysed by iron and some species are scavenged by ascorbic acid. The
aim of this work was to assess iron and ascorbic acid in uninvolved and
involved psoriatic dermis and to compare the corresponding
concentrations in the dermis of healthy subjects. Microdialysis
associated with atomic absorption spectrometry and gas
chromatography-mass spectrometry was used to assess iron and ascorbic
acid, respectively. Seven psoriatic patients and five healthy
volunteers were studied. Iron concentrations in the involved (57.1 +/-
19.3 microg/l) and uninvolved (49.7 +/- 27.1 microgl/l) psoriatic
dermis were higher than the corresponding value determined in the
dermis of healthy subjects (21.8 +/- 2.4 microg/l) (p<0.05). Ascorbic
acid in involved (47.3 +/- 8.2 microg/ml) and uninvolved (42.0 +/- 14.0
microg/ml) psoriatic dermis was statistically lower than that found in
healthy dermis (176.8 +/- 29.0 microg/ml) (p<0.05). These results
demonstrate that psoriatic patients exhibit high iron and low ascorbic
acid concentrations in the dermis, but there were no significant
differences between involved and uninvolved skin.
PMID: 15040469
Doesn't this spell it out? We have high iron and low ascorbic acid
(vitamin C). My ip6 trial should be helping to lower the iron as i'm
eating the greatest source of iron (meat) every day now. Even twice a
day. This would have flarred me to no end, had i not been using the
ip6.
But look at the ascorbic acid. It's low for us and we have high iron.
Vitamin C (ascorbic acid) sucks the iron in. IOWs you absorb more iron
from meat when you have vitamin C in your gut etc.
So, i'm putting more C into me/my skin and blocking iron from getting
there!
Something is going right. I'm getting clearer...
It's pretty darn funny how quiet's it's been around here.
Are the former pharma shills for the grand and glorius bioLOGICALS gone
now?
Don't get me wrong. I'm not down on you clearing yourselves with them.
I'm just chagrined when it comes to the PRICES they charge. We are
mentally beat down like dogs to begin with and then you have to pay a
small fortune to get clear and you wait for the inevitable again.
LIke being a slave and your set free for some time period that will
exPire like clock work. Free for 3, 6, 6, 12 months isn't really free
or cured at all.
Could two really cheap suPPlements clear you as much as the
BIOlogicals?
(Maybe not as i'm on a host of other things that now need to be taken
out to find
their usages in this trial.)
Can you imagine no more derm aPPointments?
Lets work on this some more.
Iron absorption and loss in psoriasis.
Keszthelyi B, Kiss AM, Toth A, Novotny S, Botos I.
59Fe absorption has been studied in psoriatics to elucidate the iron
deficiency state. To determine the rate of iron loss, elimination of
injected 59Fe was measured. In psoriasis mean iron absorption did not
differ from the mean in the normal group, but a pathologically low
absorption was found in 8 cases. Iron loss was significantly higher in
psoriatics than in normal men, while it did not differ significantly
from iron loss in women with regular menses.
PMID: 1030566
Fe (iron) and Zn is zinc. Ca is calcium. Ca++ is ionic ca, or is that
doric? lol
Estrogen activity lowers psoriasis. IOWs high estrogen is correlated
with less P in menstruating women. If i'm reading the abstracts right.
This is for cruiser. I asked him to check it out. But beat him to it.
lol
Back to zinc and iron now. Who didn't take zinc till it came out their
ears back in the day when some naturopath said it was the secret
treatment?
We even have zn in our shampoo's. Well some of us do.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3541156
(...)
Zn and Fe have been shown to reside mainly in the basal cell layer of
the normal epidermis but are found in high amounts in the outer cell
layers of the epidermis in hyperproliferative paralesional psoriasis.
PMID: 3541156
Lets look at the areas or zones in the skin.
http://www.vetmed.uni-muenchen.de/anat2/EpiMehrverhPlat.jpg
Whoops wrong language.
This is a little better,
http://www2.ma.psu.edu/~pt/skin.jpg
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10086851
Elemental analysis mirrors epidermal differentiation.
Forslind B, Werner-Linde Y, Lindberg M, Pallon J.
Experimental Dermatology Research Group, Medical Biophysics, MBB,
Karolinska Institute, Stockholm, Sweden. bo...@mango.mef.ki.se
Using a scanning nuclear microprobe, the distribution of elements and
trace elements of skin cross sections of normal skin, non-lesional
psoriatic skin and in dry atopic skin have been mapped. In non-lesional
psoriatic skin and in dry atopic skin the epidermal Ca-gradient is
higher than that of normal skin. In addition, abnormally high Fe and Zn
levels were recorded in the stratum granulosum and corneum regions in
the pathological skin. It is suggested that these findings correlate to
an increased cell turnover in the basal cell layer of the psoriatic and
atopic skins. The ratio of Ca/Zn in stratum corneum of paralesional
psoriatic skin is approximately 8:1 compared to 12: 1 in normal skin
and 15: 1 in atopic skin. This suggests that the differentiation
process in paralesional psoriatic skin may actually be an example of
disturbed programmed cell death.
PMID: 10086851
I never ever got better p wise by taking zinc. I may have prevented
some colds. <g>
This shows some P skin layers,
http://www.fda.gov/fdac/features/2004/504_psoriasis.html
And we need some iron (Fe) to make haem,
http://www-leeper.ch.cam.ac.uk/TetrapyrroleBiosynth/HaemBiosynth.html
http://www.google.com/search?hl=en&lr=&oi=defmore&defl=en&q=define:Heme
For you CSI types who are in to Luminol testing,
http://caligula.bcs.deakin.edu.au/bcs_courses/forensic/Chemical%20Detective/Luminol_test.htm
For people who like pictures,
http://www.fortunecity.com/greenfield/rattler/46/images/Haemoglobin.gif
Ok, so whats uP with HO-1 and P then?
Haem oxygenase-1: a novel player in cutaneous wound repair and
psoriasis?
Hanselmann C, Mauch C, Werner S.
Institute of Cell Biology, Swiss Federal Institute of Technology,
Honggerberg, CH-8093 Zurich, Switzerland.
Haem oxygenase (HO) is the rate-limiting enzyme in the degradation of
haem. In addition to its obvious role in iron metabolism, a series of
findings indicate an important role for HO in cellular protection
against oxidative stress. This effect might be of particular importance
during wound healing and also in inflammatory disease. Therefore we
determined the expression of the two HO isoenzymes, HO-1 and HO-2,
during the healing process of full-thickness excisional wounds in mice.
We show a remarkable induction of HO-1 mRNA and protein expression
within three days after skin injury. After completion of wound healing,
HO-1 expression declined to basal levels. By contrast, expression of
HO-2 was not significantly modulated by skin injury. In situ
hybridization and immunohistochemistry revealed high HO-1 expression in
inflammatory cells of the granulation tissue and in keratinocytes of
the hyperproliferative epithelium. A strong overexpression of HO-1 was
also observed in the skin of patients suffering from the inflammatory
skin disease psoriasis. In addition, HO-2 mRNA levels were increased in
the skin of psoriatic patients. Similar to wounded skin, inflammatory
cells and keratinocytes of the hyperthickened epidermis were the major
producers of HO-1 in psoriatic skin. In vitro studies with cultured
keratinocytes revealed a potential role for reactive oxygen species
(ROS), but not for growth factors and pro-inflammatory cytokines, as
inducers of HO-1 expression in inflamed skin. Our findings suggest a
novel role for HO in wound healing and inflammatory skin disease, where
it might be involved in haem degradation and in the protection of cells
from the toxic effects of ROS.
PMID: 11171041
Is psoriasis not only shedding iron but doing it in a compensatory
healing fashion?
Why stop that? Because the damn stuff doesn't stop itself, i hear you
say.
Good enough.
Maybe not. We are still at risk for complications,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8407074
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1764360
And this looks ominous,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3508446
Hyaluronic acid degradation by ascorbic acid and influence of iron.
Fink RM, Lengfelder E.
Institute of Radiation Biology, Ludwig-Maximilians-University, Munich,
F.R.G.
The effects of ascorbic acid, iron and ADP on hyaluronic acid, a
compound present in inflamed joints, were investigated in an in vitro
system. Ascorbic acid induces degradation of hyaluronic acid which
increased in the presence of FeCl3 and which is additionally stimulated
by ADP chelated ferric ions. The hyaluronic acid degrading reactions
induced by the Fe-III/ADP/ascorbic acid system were inhibited by
catalase and formate to various extents whereas the presence of
superoxide dismutase did not exert any inhibitory effect.
Desferrioxamine, a specific iron chelator, completely inhibited
hyaluronic acid depolymerisation by ascorbic acid as well as in
combination with FeCl3 or FeCl3/ADP, respectively. We suggest that the
ultimate hyaluronic acid degrading species is OH, generated via the
Fe-III/ADP catalysed Haber Weiss reaction. There is also an indication
for the involvement of perferryl or/and ferryl species in the
degradation process.
PMID: 3508446
But is it? If you continue to consume those things that make HA are you
thusly in the CLEAR?
I've continued to take glucosamine and chondroitin sulphates as they
seemingly worked nearly as well as eating the more expensive HA
suPPlements.
So, is that the secret to my success?
randall... I don't know. But i doubt it's the boron! Iron yes. Boron
NO! HA maybe!
barry...@yahoo.com.au
menstruating women.
Wouldn't they also have low iron?
Barry
randall
Does make sense. Can you make that moisturizing cream?
Or recommend one? One that i can just plunk some Ip6 into?
randall
>
> Barry
Cruiser
"randall" <ranh...@aol.com> wrote in message
news:1128877385....@z14g2000cwz.googlegroups.com...
> Ok, i'm going in reverse now. :(
>
> Right knee, elbows and ankles plaquing back up. :(
>
Sympathies.
> So, i'm doubling the dose of IP6. My trial has been dictated by the
> P, once again.
>
> Most everything else is the same.
>
> Could you look over these links cruiser?
>
I looked.
> Try to get a feel for what i'm thinking please?
>
>
It would help if you explain.
> http://www.jstage.jst.go.jp/article/bpb/28/4/28_764/_article
>
>
http://groups.google.com/group/sci.life-extension/browse_thread/thread/99aa4b15d952782a/0179bbb525d016d2?hl=en
>
> http://www.jstage.jst.go.jp/article/bpb/28/4/764/_pdf
>
>
> Can you see how i'm conflicted now with these obvious anomalies between
> C and IP6?
>
The link, that I posted for you a couple times now, and which you have
chosen to ignore, says that high dose vitamin C regulates iron levels.
So if you have low iron, yes high dose vitamin C will cause an increased
uptake. However, if you have high iron levels, high dose vitamin C will
cause the body to excrete iron. The quote is from a doctor who has seen
if work repeatedly. He suggests that high dose vitamin C may be a good
way to down regulate excess iron levels.
>
> Are you thinking now?
>
I guess you want to use an IP6 cream.
> > Yet your P levels are so low to begin with, even a tiny clearing could
> > be a huge difference to someone that's 50% or more covered.
> >
> > Say your 2-4% (? i'm guessing now) only does a 25% clearing.
> >
> > That would mean a lot more to someone that's 75% covered. But maybe
> > not that much to someone whose mild to begin with.
> >
Everything is stablized for me now. I have not developed any new plaques,
for a couple weeks, and the ones that I have are not getting any worse, yet.
If anything they may be improving.
Since you brought up cancer, here is something I missed the first time I
read
the interview.
-----------------------------------------------------
http://www.virusmyth.net/aids/data/heinterviewhk.htm
It was also possible in animal experiments to prompt tumor cells as well as
metastases to disappear completely by stimulating synthesis of NO gas.
*******Undoubtedly the most impressive is the success in healing cancer by
balanced high-dosages of cysteine and glutathione to regulate the potential
for redox by means of preparations with good bioavailability.*******
------------------------------------------------------
Cruiser
Cruiser
>
> Hey!
>
> Cruiser did you read the previous post in this thread?
Yes, sorry, I spent the weekend doing more research when
I had the time between feasting. It was Canadian Thanksgiving.
I had three days of feasting, with family.
>
> The skin is used to shed iron. P must shed a sh*t load of it.
>
OK I missed that bit. Did you figure that out yourself, or was there
a reference for that.
> Do you figure that ip6 cream right in the plaques will do more then
> just eating
> it?
I am still thinking that the benefit of IP6 is donating phosphate
groups. That is just an opinion. If you think it will work in another
way, go for it. I am trying to keep an open mind through all this.
> In my current trial i'm eating meat like crazy and normally i would be
> shedding Psoriasis like crazy. Not now. How come i'm not the usual
> major flake that
> I would be by eating the way i am? Well...?
>
> But i've started to go a little bit backwards and that means my P is
> going forwards some. :(
>
> Just a little ok.
>
> What should i do?
>
Keep up what your search and trials and let us know how it works out.
You have posted so much information, that I will take a long time
to wade through it all.
Cruiser
randall
Cruiser wrote:
> "randall" <ranh...@aol.com> wrote in message
> news:1128976473.2...@f14g2000cwb.googlegroups.com...
> >
> > Hey!
> >
> > Cruiser did you read the previous post in this thread?
>
> Yes, sorry, I spent the weekend doing more research when
> I had the time between feasting. It was Canadian Thanksgiving.
> I had three days of feasting, with family.
>
Well, i didn't know you guys had yours so much earlier then us.
Have noticed the price on turkeys moving down. :)
You do get colder then us sooner. So your p may trigger a little
differently in that regard. Provided there is a there there.
> >
> > The skin is used to shed iron. P must shed a sh*t load of it.
> >
>
> OK I missed that bit. Did you figure that out yourself, or was there
> a reference for that.
Yeah, four or five posts back,
http://www.fsm.ac.fj/Medicine%20Website/HADIF%20website/12%20Anemia/12-%20Anemia.htm
Four or five chapters on it.
>
> > Do you figure that ip6 cream right in the plaques will do more then
> > just eating
> > it?
Yes. According to that pdf from the UK we can get double or triple
the amount in. And according to some of those abstracts that
looks right to make up deficits.
I'm stoked. Well, when i find a neutral moisturizer to act as the
delivery system, my skin plaques will be. Recall that i'm nearly
plaqueless at this time.
My one gram a day is working to knock back down the current re-flakery.
<g>
>
> I am still thinking that the benefit of IP6 is donating phosphate
> groups. That is just an opinion. If you think it will work in another
> way, go for it. I am trying to keep an open mind through all this.
All those abstracts in the last two days nail it. Well enough for me.
Well enough for many of us i'm hoPing as well.
>
> > In my current trial i'm eating meat like crazy and normally i would be
> > shedding Psoriasis like crazy. Not now. How come i'm not the usual
> > major flake that
> > I would be by eating the way i am? Well...?
> >
>
> > But i've started to go a little bit backwards and that means my P is
> > going forwards some. :(
> >
> > Just a little ok.
> >
> > What should i do?
> >
>
> Keep up what your search and trials and let us know how it works out.
>
> You have posted so much information, that I will take a long time
> to wade through it all.
Sorry, but i got excited. Trying to figure out what's the positive
factors in this trial didn't just pop in to my head. I had to sleep
on it, ruminate and stuff my face with a ton of meat.
Then i had to realize the shortfalls of my LPS theory. Maybe it only
spurs th1 cells and nothing more. Which is a lot.
Otherwise the culprits have to be right under our nostrils.
Provided thats where your plaques are.
randall...well well, there there, where? Clear yet? :)
>
> Cruiser
randall
Cruiser wrote:
> "randall" <ranh...@aol.com> wrote in message
> news:1128877385....@z14g2000cwz.googlegroups.com...
>
> > Ok, i'm going in reverse now. :(
> >
> > Right knee, elbows and ankles plaquing back up. :(
> >
>
> Sympathies.
Almost back to the same clear progress in just a few days of
one gram a day. :)
Please realize this trial was designed to fail. I need no
sympathies as i expected to fail before now. I stumbled in to
the vitamin C thing after talking one day with Bill Sardi.
One or two emails and I now owe my current success to those
moments of Aha!
>
> > So, i'm doubling the dose of IP6. My trial has been dictated by the
> > P, once again.
> >
> > Most everything else is the same.
> >
> > Could you look over these links cruiser?
> >
>
> I looked.
>
> > Try to get a feel for what i'm thinking please?
> >
> >
>
> It would help if you explain.
>
> > http://www.jstage.jst.go.jp/article/bpb/28/4/28_764/_article
> >
> >
> http://groups.google.com/group/sci.life-extension/browse_thread/thread/99aa4b15d952782a/0179bbb525d016d2?hl=en
> >
> > http://www.jstage.jst.go.jp/article/bpb/28/4/764/_pdf
> >
Easy, the IP6 besides affecting cancer pathways (Phosphoinositide
3-kinase (PI 3-K) , it may be helping the psoriasis skin zones to
re-normalize
with vitamin C and the ratio's of minerals.
All the abstracts on minerals in the last few days of posts. :)
> >
> > Can you see how i'm conflicted now with these obvious anomalies between
> > C and IP6?
> >
>
> The link, that I posted for you a couple times now, and which you have
> chosen to ignore, says that high dose vitamin C regulates iron levels.
And i've said to you many times now, that every time in the last three
decades that i used mega-dose Vitamin C it lead to more P.
Only now combo'd with IP6 has the ability to get in to the pearly gates
become aPParent.
Combo sombo, it's JXstern's freaking cocktail alrighty now. lol
It's the vitamin C and IP6 cocktail. You just have to wait an
hour after taking the IP6 on an emPty stomach before you go with the C.
A cocktail with a C shot an hour back. lol
One modification now is taking the c shot right before one
of my two meals. Not after. But after if i forget.
>
> So if you have low iron, yes high dose vitamin C will cause an increased
> uptake. However, if you have high iron levels, high dose vitamin C will
> cause the body to excrete iron. The quote is from a doctor who has seen
> if work repeatedly. He suggests that high dose vitamin C may be a good
> way to down regulate excess iron levels.
>
And now we know there may be great magic in that. I just have to back
all those other suPPlements out to find which ones are augmenting
this new found clearness.
> >
> > Are you thinking now?
> >
>
> I guess you want to use an IP6 cream.
May not be required. Then again may take one there even quicker!!!
Who would be against that?
Not even uwe! Free help for all psoriatics!
The promise land is just across the river jordan. lol
Thats how they must feel in the gaza striP right now. <g>
>
> > > Yet your P levels are so low to begin with, even a tiny clearing could
> > > be a huge difference to someone that's 50% or more covered.
> > >
> > > Say your 2-4% (? i'm guessing now) only does a 25% clearing.
> > >
> > > That would mean a lot more to someone that's 75% covered. But maybe
> > > not that much to someone whose mild to begin with.
> > >
>
> Everything is stablized for me now. I have not developed any new plaques,
> for a couple weeks, and the ones that I have are not getting any worse, yet.
> If anything they may be improving.
>
So, in your list of stuff, what is it that's doing that? I'm betting
on
the ip6. Take it out and leave the C in and see for yourself.
You flare, you now know it's the ip6 that has its finger in the dike.
> Since you brought up cancer, here is something I missed the first time I
> read
> the interview.
>
> -----------------------------------------------------
> http://www.virusmyth.net/aids/data/heinterviewhk.htm
Oh man, every time i go back to this virusmyth pages, it brings up
the association with uwe and big conspiracies.
Should I have not wanted to freely give of myself in the P clearing
project, I could be as screwed up as uwe right now.
What I realized from him is that everyone in this P game. Derms,
pharma's
us, them etc are all uwe's. We want a one pill cure, the pharm's want
to milk us forever and I want to clear you and me tomorrow.
Whose gonna win? Not uwe, that's for sure. Whose gonna buy his
fly on over and i'll cure you routine?
I'll take an ignoble prize and be happy once i'm CLEAR and at least
a million of you out there.
Then i'll call Kerry Mullis and get a picture with him holding his
prize
for PCR.
I'll have worked on mine 99 times longer then it took him
to get his nobel. And I had to live with the P consequences while i
did.
We can go surfing and i'll not wear the wetsuit.
Nice clear skin in the deeP blue sea.
Now thats a dream. Will it come true?
Not if some of you out there don't jump on the wagon!
Are you all shills for the pharma's? I hope not.
I'll have to spend more time and money to get the message out.
But why not? It's been a labor of love.
I may as well go thru the labor to push the kid out. lol
>
> It was also possible in animal experiments to prompt tumor cells as well as
> metastases to disappear completely by stimulating synthesis of NO gas.
> *******Undoubtedly the most impressive is the success in healing cancer by
> balanced high-dosages of cysteine and glutathione to regulate the potential
> for redox by means of preparations with good bioavailability.*******
>
I got off on NO gas how many times?
Try a randall nitric oxide search of the P ng.
Toss in you for the posts only with you, should you wish.
Btw, thanks for your inPut,
randall.. where? there! my plaques use to be there! I see none! IP6
> ------------------------------------------------------
>
> Cruiser
Cruiser
Randall,
http://www.cdc.gov/hemochromatosis/training/glossary.htm#H
---------------------------------------------------------------
Hemochromatosis:
The disease that occurs as a result of significant iron overload.
Hemochromatosis can have genetic and nongenetic causes.
---------------------------------------------------------------
http://www.biochem.northwestern.edu/holmgren/Glossary/Definitions/Def-F/ferritin.html
ferritin:
The primary form of storage iron.
---------------------------------------------------------------
http://www.vitamincfoundation.org/faqdocs.html
Q. Orthodox medicine advises people with Hemochromatosis (congenital iron
overload in tissues) to avoid vitamin C? What is the foundation's opinion?
The foundation understands that vitamin C facilitates iron absorption, but
according to our advisors, it also helps to regulate unbound Iron out of the
body and might be a good treatment for this condition. People with
hemochromatosis can take steps to reduce iron in the digestive tract at the
same time they are taking vitamin C orally.
A., Opinion of Robert Cathcart, III, MD (orthomed.com) :
My clinical experience would indicate that vitamin C increases iron
absorption when iron is needed. It seems to increase excretion of iron when
there is an excessive amount of iron. Therefore, vitamin C might be a good
treatment of hemochromatosis.
This theoretical difficulty concerning C is typical of how the orthodoxy
will expand a theory into a fact without any evidence.
docc.
A. Selva Kumar, MD opinion
I have managed many cases of iron overload because I see many Thallasaemia
trait cases where the older patients usually have anemia but high ferritin
levels. I continue giving 30 grams sodium ascorbate infusion weekly or
biweekly for their chronic conditions, yet their ferritin DID NOT INCREASE
and you see improvement in their anemia, with added folic, vitamin E and
oral vitamin c at 3 to 6 grams per day.
----------------------------------------------------------------
Not sure of the path that iron uses to exit when vitamin C "helps to
regulate
unbound Iron out of the body".
Cruiser
randall
Not only that but i need to knock down the level's of meat i'm
eating. I can only imagine what my BP is looking like. :(
randall.. all to gain a little clearness
Cruiser
I also found this.
-----------------------------------------------------
http://www.positivehealth.com/permit/Articles/Nutrition/vitc2.htm
Vitamin C is one of the main promoters of dietary iron absorption, along
with meat and fish(96). Vitamin C can form soluble iron complexes and reduce
ferric to ferrous iron. The main dietary inhibitors of iron absorption are
phytates found in pulses and polyphenols(96). Tea, and to a lesser extent,
coffee, inhibit iron absorption(183). Vitamin C's enhancement of iron
absorption is normally regarded as a positive attribute; nevertheless,
concerns have been raised postulating that Vitamin C could have the effect
of increasing iron absorption so much as to cause excessive iron or iron
overload.
According to Rivers who recently reviewed the research evidence "the
regulatory mechanisms that control body iron stores override any pronounced
alterations in food iron availability...Concern that massive doses of
ascorbic acid might lead to pressive iron accumulated in healthy
iron-replete individuals appears unwarranted"(178).
In fact research indicates that Vitamin C can actually help to reduce
excessive iron stores in individuals with iron-overload disorders. Such
individuals have subnormal white blood cell levels of Vitamin C, caused by
their excessive iron storage. When Vitamin C is administered to restore
normal white cell levels excessive iron is excreted(231).
Therefore the evidence seems to point to Vitamin C having a pivotal
homeostatic role with respect to iron - it promotes iron absorption in
iron-deficient individuals and accelerates iron excretion in people with
excessive iron.
-------------------------------------
Also, I found a bunch of references that say Alpha Lipoic Acid increases
urinary iron excretion.
You may want to add ALA to your supplements, to see if that helps.
Cruiser
randall
also. I am on it and was thinking last week about adding in
ALC, the other half of alcar.
And the Racemic version of ALA as well. Up till now the old
DNA wasn't headed south so fast.
May as well try to slow down time. lol
randall.... what is time? Whoops gota go!
cruiser
-----------------------------------------------------------
http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/rib_0263.shtml
Boron: Boric acid may induce riboflavin deficiency, since it displaces
riboflavin from plasma-binding sites and results in increased urinary
excretion of the vitamin. Most forms of boron (see Boron) used for
nutritional supplementation are readily converted to boric acid. High
intakes of these boron supplements may result in riboflavin deficiency.
------------------------------------------------------------
Cruiser
Cruiser
-----------------------------------------------------------
http://www.scielo.br/scielo.php?pid=S1516-635X2004000400004&script=sci_arttext&tlng=en
Rossi et al. (1990) reported the effects of four boron levels (0, 20, 80 and
320 ppm) combined with two levels of riboflavin (4.4 and 17.6 ppm) in the
diets of broiler chickens from 1 to 49 days. At 21 days of age, feed intake,
body weight and mortality were significantly lower for broilers given 320
ppm boron in the diet. Besides, broilers fed diets containing boron had
better feed conversion in the experimental period when compared to the
control group (0 ppm boron). The three tested boron levels had no effect on
tibia weight and ash content. The highest level of riboflavin in the diets
did not compensate for the adverse effects of the highest boron level on
body weight. However, lower boron levels combined with riboflavin resulted
in a significant improvement in broiler body weight at the end of the
experimental period.
------------------------------------------------------------
Cruiser
"cruiser" <tg.cr...@sympatico.ca> wrote in message
news:IAB5f.21285$GH1.4...@news20.bellglobal.com...
Enna123
anxiety. Since neurotransmitters like serotonin depend on inositol to
function, it may play an important role in preventing and eliminating mood
disorders. Clinical evidence suggests that large doses (12-18 grams) of
inositol can decrease the frequency and severity of panic attacks, improve
symptoms of depression and increase attention in patients with attention
deficit disorder.
http://www.herbs-wholesale.com/Inositol/328/1/Inositol.htm
Pete
Brufen per day. During this time, my psoriasis massively flared and
spread quickly to new sites all over my body. Since ceasing the
medication the flaring and spreading is settling. I have never been so
itchy.
To date, I have not found my psoriasis to be affected by what I eat but
it is surely exacerbated by NSAIDs.
Can some enlightened person explain for me what is happening
biologically here. A google search establishes this as anecdotally
reported for some people but not others who may in fact use NSAIDs for
management of psoriatic arthritis. I am curious if this response points
to a particular pathway for *my* psoriasis that might also offer points
of intervention.
Thanks all.
Peter.
randall
Pete wrote:
> I fell down the stairs injuring my back and for a week I was on 1600 mg
> Brufen per day. During this time, my psoriasis massively flared and
> spread quickly to new sites all over my body. Since ceasing the
> medication the flaring and spreading is settling. I have never been so
> itchy.
Find the itch site and look for clues as to your symptoms. Did your
derm or
doc offer any explanations?
Here's the medscape for P and itch,
http://www.medscape.com/viewarticle/541971?rss
Here's the itch site,
http://www.aafp.org/afp/20030915/1135.html
Here's a pdf of the same site.
http://www.aafp.org/afp/20030915/1135.pdf
I found an abstract that may let you know your not alone.
Now I can't find it. lol
So, widen the search,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&dispmax=100&term=%20pruritis+psoriasis
And then try nsaid* + Itch* and here it is,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8933896&query_hl=8&itool=pubmed_docsum
Not psoriasis and itch, but atopy isn't to far from our pathways.
Since i've added supplements in to my program, I can eat more formerly
inflammatory
foods (AA) without increasing psoriasis activity. But present activity
(sub 3% at present) is much more itchy. Must be a consequence of
arachidonic acid (AA) and HA or something
like that.
>
> To date, I have not found my psoriasis to be affected by what I eat but
> it is surely exacerbated by NSAIDs.
Sure sounds like diet is a factor in your present situation.
Always was and is in mine. Try fasting and starvation to confirm.
Take out all arachidonic acid foods. (Pork, dairy, red meat, poultry
fish etc... and eliminate n-6 oils like soy bean oil, corn oil and only
use olive oil and sparse amounts of canola. And take one tablespoon
a day of flax seed oil and fish oils or cod liver oil.
Or become a vegetarian for a few months. You'll know fairly quickly.
If not then add in some keywords to this search,
http://groups.google.com/groups/search?q=pruritus+psoriasis&qt_s=Search
or
http://www.clevelandclinicmeded.com/diseasemanagement/dermatology/pruritus/pruritus.htm
&
http://en.wikipedia.org/wiki/Itch
Try histamine and AA,
http://www.google.com/search?hl=en&lr=&q=pruritus+arachidonic+cox-2+histamine&btnG=Search
>
> Can some enlightened person explain for me what is happening
> biologically here. A google search establishes this as anecdotally
> reported for some people but not others who may in fact use NSAIDs for
> management of psoriatic arthritis. I am curious if this response points
> to a particular pathway for *my* psoriasis that might also offer points
> of intervention.
With dietary restrictions as confirmation, it points up arachidonic
acid at work.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&dispmax=100&term=%20arachidonic+pruritis
While YOU may not have noticed diet at work, it takes a lifetime for
the effects.
TAke the stress post yestereday.
Some folks have good dna and simply live long.
http://www.cbc.ca/story/world/national/2006/08/28/oldest-woman.html
Was it the wine or donkey milk? lol
Dairy for us is usually a problem. If that isn't dna what is?
So, stress increases cortisol and the inflammation cycle is fed.
http://www.signonsandiego.com/news/health/20060829-9999-lz1c29stress.html
Anything in the enviroment or taken orally is suspect. We don't live in
a vacuum or outer space. <w>
If we never onset with P, the arachidonic acid from our diets would
contribute
to a shorter life via other pathways influenced by arachidonic acid.
If one wishes to call arachidonic acid an allergen for the psoriatic 2%
then
be my guest.
http://www.google.com/search?hl=en&lr=&q=pruritus+arachidonic+allergen&btnG=Search
But why could we eat it without problems before onset?
Which raises the question for the 101th time. Is psoriasis compensatory
for
inflammation? Is the skin only acting as an organ of elimination?
randall... my 2 cents off the toP of my head anyway.
>
> Thanks all.
>
> Peter.