Another remedy bites the dust?
skeatsan''co
in trials so probably the same goes for psoriasis too?
Information from the BBC Health pages
http://news.bbc.co.uk/1/hi/health/3314753.stm
Includes following:
................................"After 12 weeks, their eczema symptoms -
skin rashes - were reviewed to check for signs of improvement.
There was a slight improvement in the starflower oil group - but a bigger
improvement was noticed among the placebo group, who had received no herbs
or medicines at all.
There was no evidence that those on starflower oil used a smaller quantity
of steroids as a result.
The conclusion was a plain one - that linolenic acid, the principal active
ingredient, was "not
beneficial".............................................
JXStern
First, they're talking eczema, not psoriasis, of which one might be a
Th2 malfunction and the other a Th1.
You have to control for diet or you can't even run a study like this.
Maybe GLA does nothing for eczema, I didn't always read evetsm's
postings and conclusions.
But for psoriasis, I can turn symptoms visibly on and off over just a
few hours by taking a 500mg capsule -- depending on what other drugs
and diet I've been on. And, longer term, the primrose oil has cleared
nails for me and at least a few others on this newsgroup, where that
can otherwise be a huge problem.
All that means is that there are *some* patients whose condition and
constitution and diet enable the given treatment to work. We know
from this group that primrose oil does nothing for lots of people as
well. In a sloppy study, that just dilutes the numbers from the
subset of people for whom it is effective. A good study will find the
criterion to pre-select those for whom it might work, and then confirm
that it does.
I find this "bites the dust" by them very unprofessional and certainly
unwarranted by any single study, and makes me wonder if they biased
the experiment against positive results from the start.
J.
Randall
> Starflower and Primrose oil didn't do any better that the placebo for eczema
> in trials so probably the same goes for psoriasis too?
EPO and borage never did anything for me positive.
When i found out they were mainly omega-6's (ALA) i
knew the fix was in somewhere as n-6 never did more then
add fuel to the fires.
I still see red just thinking about them. yikes!
>
> Information from the BBC Health pages
> http://news.bbc.co.uk/1/hi/health/3314753.stm
> Includes following:
> ................................"After 12 weeks, their eczema symptoms -
> skin rashes - were reviewed to check for signs of improvement.
>
> There was a slight improvement in the starflower oil group - but a bigger
> improvement was noticed among the placebo group, who had received no herbs
> or medicines at all.
Why did they allow a confounder (the herbs) into the study in the
first place?
>
> There was no evidence that those on starflower oil used a smaller quantity
> of steroids as a result.
Another GIANT confounder, steroids!
What kinda flaky study was this?
>
> The conclusion was a plain one - that linolenic acid, the principal active
> ingredient, was "not
> beneficial".............................................
Ok, let me read this myself,
"The conclusion was a plain one - that linolenic acid, the principal
active ingredient, was "not beneficial".
Open debate
Professor Hywel Williams, from the Centre of Evidence-based
Dermatology at Queen's Medical Centre in Nottingham, said that the
largest and best studies on the subject of gamma linolenic acid, the
ingredient of starflower and evening primrose oils, had shown no
convincing evidence of benefits against dermatitis.
=================================
I can hear JXStern now,
But but but. lol
Gla and DGLA must do something for someone with P?
I know the ALA/LA is bad? I can hear J now. lol
Though, i recently figured that CLA (a fraction of omega-6 which is
alpha
linolenic acid -ALA) may help some (see the downunder doctors that
fractionated
out 40 to 50 fractions from ALA, thread) i'm starting to think its
doing
the reverse of what i would expect for my psoriasis.
Even in the face of all the abstracts i posted on it.
Apparently we p's don't conform to the medical abstracts out there
for CLA, regardling inflammation.
While i've hoped that i would lose weight and gain energy (i have on
both accounts) i also secretly prayed for some skin clearings.
I'm only a week into this trial and taking one gram (1000mgs) a day
of tonalin CLA and i'm almost positive its causing new P plaques.
EVEN, on top of using the wheatgrass spray. Now this is a hard
one to figure as all the abstracts point to the exact opposite
scenario then what i'm experiencing.
I will be cutting way back on CLA. Down to every other or third
day, or quitting and tossing the rest down the drain.
I know i've said avoid all omega-6 (ALA) as much as possible
and this rather inexact study seems to bear that out.
(Still, can you imagine testing a biologic and still be
using some steroids? I can't!)
Yet, flax seed oil (FSO) contains omega-3 and -6's, just
enough -3's to counterbalence the -6's hopefully.
Maybe a 3:1 ratio or so, iirc. So, in theory if
not reality the PPAR receptors get plugged with the
good 3's and the 6's are blocked.
So, while we are never gonna avoid all 6's that go
downsteam and become arachidonic acids in the cell
membranes and flaky plaques in the final analysis.
We can limit our consumption of every other god forsaken
vegetable oil in the pantry. Stick with olive oil only
for your main stay.
NOW, i KNOW that makes a huge difference as i would
be so severe without that knowledge that my actions
would be speaking biologics right now.
JXStern
>I can hear JXStern now,
>But but but. lol
>Gla and DGLA must do something for someone with P?
>I know the ALA/LA is bad? I can hear J now. lol
Yo.
Randall, didn't you have something postive to say about GLA recently,
even if it was just theoretically, and only for those with type J
metabolisms?
Don't make me google ...
J.
lurknowhere
unique to our immune system: they dampen the TH1 (T helper cell 1) response.
The immune system has a variety of cells that react when bacteria or viruses
get into our bloodstream, and one important cell is the T-cell. There are
various types, classified by the cytokines (type of molecules) they release.
One pattern of molecules that comes out of T-cells is called the TH1
pattern - molecules that tend to activate macrophages (cells in our body
that chew up, swallow, and kill various bacteria). Theses include interferon
gamma (IFN-g), and tumor necrosis factor alpha (TNF-a). Most bacteria, and
viruses stimulate a TH1 response. What worms do is dampen this repsonse, and
enhance another pathway, called TH2 (T helper cell 2) that involves
eosinophils (a type of immune cell), different types of antibodies, and
different types of molecules.
Inflammatory bowel disease is predominantly a TH1 response. What we
hypothesized is that we are no longer being exposed to worms that dampen our
TH1 response and stimulate TH2 - this is a very unique property of worms.
When we lost our worms, we may have eliminated one of the few environmental
factors that dampen TH1 and prevent inflammatory bowel disease. For the
first time in our evolutionary history children were being raised without
worm exposure beginning in the early 1900s. For instance, Jewish children
who lived in New York City in the 1930s wore shoes, traveled on cement
sidewalks, did not eat the contaminated pork and therefore did not acquire
worms like most other Americans. They were the first to develop IBD. As
people became cleaner and cleaner in the North, where the climate is colder
and it is easier to avoid these organisms, IBD spread. Then, as the southern
part of the United States began cleaning up, people there started getting
the disease. In South Korea and Japan there is now an epidemic of IBD.
Whites in South Africa are getting it. Israeli Jews but not Israeli Arabs
are getting it, etc., etc. If you simply follow IBD around the world,
wherever there is de-worming you are seeing a rapid rise in IBD frequency.
It occurred to us that worms may be a critical environmental factor - that
the loss of this natural dampening influence (of worms) has resulted in many
of us becoming hyper-reactive. When we get exposed to bacteria and viruses,
we tend to over-respond, and some of the protective immune systems of the
gut mucosa that prevent uncontrolled inflammation start breaking down."
http://www.newtreatments.org/Bowel/ga/433/Crohn's%20and%20Colitis%20finally%
20cured:%20Absence%20of%20worms%20causes%20inflammation
Just fishing for answers...
-lurk
"JXStern" <JXSternC...@gte.net> wrote in message
news:7tqrtvo4c1rm9qrui...@4ax.com...
JXStern
<lakstheo...@wolfmark.com> wrote:
>"What makes the worm an important candidate is that they do something very
>unique to our immune system: they dampen the TH1 (T helper cell 1) response.
Well if that's true, then our bodies adapted to produce TOO MUCH Th1,
so that we're mostly OK even with worms suppressing it.
This is good news, because now we can come up with drugs to do the
same, decrease Th1 suppression, and know that it won't *really*
comprimise the immune system, just bring it back in balance!
Meanwhile, maybe I'll go have some sushi.
J.
evetsm
> in trials so probably the same goes for psoriasis too?
>
> Information from the BBC Health pages
> http://news.bbc.co.uk/1/hi/health/3314753.stm
> Includes following:
> ................................"After 12 weeks, their eczema symptoms -
> skin rashes - were reviewed to check for signs of improvement.
>
> There was a slight improvement in the starflower oil group - but a bigger
> improvement was noticed among the placebo group, who had received no herbs
> or medicines at all.
I am not really that surprised with this, in light of the TH1/2 take
on atopic eczema, of which there does not seem to be too much dispute
(until there is :) )
I am currently trawling the lit. for the effects of fats on TH1/2 and
the most promising candidate for a TH1 shift is coconut oil(required
in eczema treatment). The other oils, especially the PUFA's, seem to
give a TH2 bias, which may explain J seeing improvement using GLA. The
things to look for in psoriasis are oils that shift towards TH2 and so
block or downregulate interferon gamma, il-12, il-2 and boosts il-4,
TNF, and all the other il's. eg fish oil. BUT, the highly unsaturated
PUFA's are extremely prone to oxidation and that brings a whole other
set of problems. I am not sure that oil immunotherapy is the answer.
JXStern
>I am currently trawling the lit. for the effects of fats on TH1/2 and
>the most promising candidate for a TH1 shift is coconut oil(required
>in eczema treatment). The other oils, especially the PUFA's, seem to
>give a TH2 bias, which may explain J seeing improvement using GLA.
That would be interesting, all I ever heard was that GLA lead to
different prostaglandin/cyotokine/leukotrine chemistry, but that is 50
year old science, maybe it was T-cell populations all along!
The thing is, I also seem to see some benefit from coconut, so if it
does something about a Th1 shift, maybe it does some other stuff as
well.
J.
Pieter Hoeben
>factors that dampen TH1 and prevent inflammatory bowel disease.
Yes, I see what you want to say.
But somehow I am reluctant to get worms.
Pieter
skeatsan''co
I did a Google search on the chemicals contained in Coconut oil and came up
with this page which has lots of useful information in layman's terms.
http://www.holisticbirds.com/hbn03/winter03/pages/coconutoil.htm
(It even has been used to get rid of intestinal worms which links with my
other thread "Yuk..........................")!
Skeatsan''co
Randall
> On 15 Dec 2003 11:07:02 -0800, ranh...@aol.com (Randall) wrote:
> >I can hear JXStern now,
> >But but but. lol
> >Gla and DGLA must do something for someone with P?
> >I know the ALA/LA is bad? I can hear J now. lol
>
> Yo.
>
> Randall, didn't you have something postive to say about GLA recently,
Yes, i guess i jumped the gun on CLA (conjugated linoleic acid)
as i felt so good and had all this new found energy. :)
Then the P flares caught up to me and my prospective CLA dreams
went down the drain. Sure my leptin levels may have held
off the flare for a few extra days, i'll never know.
So, for the present time (till the big fat fractions move down
the pipe and actually show me first hand) all
cla's and gla's are persona non grata in my book.
I have the same problem with the false salvation of
taking extra digestive agents. They just don't live
up to the expected hyPe. The vitamin companies are
scamming us. Pure and simple as it sounds, we've
been led down the primrose path to many times.
In theory so many many things have come and gone
with a song and a whimPer that there imPPosible
to keep track of. I look back in horror at all
the lost money that could have been put to better
use.
Yet,
I still haven't gone on scalene or CLO for the A&D vitamin
Th2 skewing possibilities. If i do and the clearing is beyond
amazing i may wade back into cla very very slowly, if at all.
While, i found tons of abstracts that pointed to inflammatory
help with CLA, i still could't take cla without P flaring. :(
I have to tell you JS that all linoleic acids (LA) screw me
fairly fast. Linolenic acids on the other hand are a life
saver. I know i can google tons of posts expressing my
amazement at your good luck with gla from epo and borage.
Flax is good. Soy, corn, safflower, epo, borage etc all
are bad for me. I'm just not a omega-6 kinda guy.
As long as i stick with omega-3's, in at least a 3:1 ratio
over the n-6's i can handle the topical dilemma no problems.
EPA and DHA from fish or flax are also A OK as to nonflares.
> even if it was just theoretically, and only for those with type J
> metabolisms?
Well of course. As you've always said, YMMV. lol
>
> Don't make me google ...
Oh the humanity! It's not like i haven't confused
linoleic with linolenic at least 5 or 6 times in over
how many hundreds of posts?
And then trying to keep those two straight as the
real facts on delta5/6 desaturases comes in is nearly
confusing enough to cause me to give up on keeping
track period.
Recent abstracts on the delta's cause me to
wonder if our unknown not clear stereo P fats
aren't working counter intuitively in these
regards also.
Can you imagine where we're gonna be with 60 fractions
of linoleic and linolenic to keep tabs on?
Now, that is scarry.
Just give me the good stuff. Pure omega-3's seem like
the fraction i'd opt for. :)
>
> J.
JXStern
...
>Yet,
...
Yet probably none of this stuff is either a cause or a cure, not even
Th* balances and worms, nor any EFA, they only help to control the
inflammatory symptoms that come from elsewhere ... maybe related to
your beloved LPS, and then again, maybe not.
Hizzle Holidizzle to all,
J.
Randall
No recipe stands alone from the primary ingredients without suffering
some loss of recognition. What all goes into P?
Plenty!
GLA isn't even on my radar for any of this.
Certainly, a condition as nefarious as P,
isn't easily concocted when the cause is so hard to define.
We can talk CLA and CLA, can't we?
Lets see what the real CLA's for P are,
Superantigens
Microbial antigens that have in common an extremely potent activating
effect on T-cells that bear a specific variable region. Superantigens
cross-link the variable region with class II MHC proteins regardless
of the peptide binding in the T-cell receptor's pocket. The result is
a transient expansion and subsequent death and anergy of the T-cells
with the appropriate variable regions.
And while gut bacteria appears to come into play with psoriasis,
the dots aren't connected all that conclusively yet,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14652821&dopt=Abstract
Still, how much superantigen do we need for P when we have some LPS
floating around to turbo charge the mixture?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12780689&dopt=Abstract
Bacteria
Unicellular prokaryotic microorganisms which generally possess rigid
cell walls, multiply by cell division, and exhibit three principal
forms: round or coccal, rodlike or bacillary, and spiral or
spirochetal.
Strep and Staph appear to be at play in the field of P. Can we say
coccoids linger and create havoc? And in this p paradigm may hold some
unknown effects from our view?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9894851&dopt=Abstract
Lipopolysaccharides
Lipid-containing polysaccharides which are endotoxins and important
group-specific antigens. They are often derived from the cell wall of
gram-negative bacteria and induce immunoglobulin secretion. The
lipopolysaccharide molecule consists of three parts: LIPID A, core
polysaccharide, and O-specific chains (O ANTIGENS). When derived from
Escherichia coli, lipopolysaccharides serve as polyclonal B-cell
mitogens commonly used in laboratory immunology. (From Dorland, 28th
ed)
What are the LPS's doing in P?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12562231&dopt=Abstract
Exposure of fibroblasts, but not KCs, to lipopolysaccharide or HSPs
triggered nuclear factor (NF)-kappaB activation. Heat shock proteins
did induce maturation of blood-derived DCs accompanied by increased
interleukin-12 production and enhanced antigen-presenting function.
CONCLUSIONS: These data demonstrate distinctive patterns of innate
immune-related receptors by specific subsets of cells in normal and
psoriatic skin, suggesting functional roles for HSPs and DCs in
psoriasis.
And LPS has its own gene for P,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12185532&dopt=Abstract
I would think we may need a few more p genes to go along with it.
Still the receptors are there, aren't they?
Lipopolysaccharide Receptors
Glycolipid-anchored membrane glycoproteins expressed on cells of the
myelomonocyte lineage including monocytes, macrophages, and some
granulocytes. They function as receptors for the complex of
lipopolysaccharide (LPS) and LPS-binding protein.
So, in the light of this/these posts please now clue me in as to how
the stereoconfiguration (12R-Hete) of the fats occurs?
http://groups.google.com/groups?q=stereoconfiguration+group:alt.support.skin-diseases.psoriasis&hl=en&lr=&ie=UTF-8&group=alt.support.skin-diseases.psoriasis&selm=df7e2c67.0312031002.63082ac7%40posting.google.com&rnum=1
And if you need another clue, look no farther then your tonsils,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11368351&dopt=Abstract
My mistake, wrong JR, wouldn't you know!
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&selm=ac3a7293.0312122145.1872ea76%40posting.google.com
No, I got better after my tonsils were removed so explain that.
We should only have one JR to a group. So JXStern isn't JR for randall
anymore. We will have no stereoconfiguration of JR's in this group.
lol You didn't even know you had a doppelganger in the p ng? lol
You do have to admit JX that that was a pretty good clue. Even if it
isn't
yours. The other not version of you caused the P genes to trigger. lol
To reveal the faces of the other genetic multifactorial P DNA players
we need go no further then gata-3 to see how Th2 is muted and our P
fate is sealed,
http://groups.google.com/groups?q=gata-3+group:alt.support.skin-diseases.psoriasis&hl=en&lr=&ie=UTF-8&group=alt.support.skin-diseases.psoriasis&selm=df7e2c67.0312141401.45185fc4%40posting.google.com&rnum=1
So, while we can name names in the P game we haven't connected the
dots yet. The recipe seems almost complete, doesn't it?
I'm more or less satisfied with what is known and suspect the
denouement will be only a clarification of all the disjointed
appearing abstracts laying around the psoriasis group.
>
> Hizzle Holidizzle to all,
Cheese thanks,
Still the LA, GLA isn't over yet,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14676141&dopt=Abstract
Cheese made of milk from cows grazed on alpine pastures had a more
favorable fatty acid profile than all other cheese types. Alpine
cheese may be a relevant source of ALA and other cardioprotective
fatty acids.
Give me the grassy cheese any day. The grassy spray also!
Why doesn't CLA make sense for P? Besides flaring me,
we have confusing abstracts coming down the pike like
this next one.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12848277&dopt=Abstract
School of Chemical and Life Sciences, University of Greenwich at
Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
L.Ha...@gre.ac.uk
The essentiality of n-6 polyunsaturated fatty acids (PUFA) is
described in relation to a thymus/thymocyte accretion of arachidonic
acid (20:4n-6, AA) in early development, and the high requirement of
lymphoid and other cells of the immune system for AA and linoleic acid
(1 8:2n-6, LA) for membrane phospholipids. Low n-6 PUFA intakes
enhance whereas high intakes decrease certain immune functions.
Evidence from in vitro and in vivo studies for a role of AA
metabolites in immune cell development and functions shows that they
can limit or regulate cellular immune reactions and can induce
deviation toward a T helper (Th)2-like immune response. In contrast to
the effects of the oxidative metabolites of AA, the longer-chain n-6
PUFA produced by gamma-linolenic acid (18:3n-6, GLA) feeding decreases
the Th2 cytokine and immunoglobulin (Ig)G1 antibody response. The n-6
PUFA, GLA, dihomo-gamma-linolenic acid (20:3n-6, DHLA) and AA, and
certain oxidative metabolites of AA can also induce T-regulatory cell
activity, e.g., transforming growth factor (TGF)-beta-producing T
cells; GLA feeding studies also demonstrate reduced proinflammatory
interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha production.
Low intakes of long-chain n-3 fatty acids (fish oils) enhance certain
immune functions, whereas high intakes are inhibitory on a wide range
of functions, e.g., antigen presentation, adhesion molecule
expression, Th1 and Th2 responses, proinflammatory cytokine and
eicosanoid production, and they induce lymphocyte apoptosis. Vitamin E
has a demonstrable critical role in long-chain n-3 PUFA interactions
with immune functions, often reversing the effects of fish oil. The
effect of dietary fatty acids on animal autoimmune disease models
depends on both the autoimmune model and the amount and type of fatty
acids fed. Diets low in fat, essential fatty acid deficient (EFAD), or
high in long-chain n-3 PUFA from fish oils increase survival and
reduce disease severity in spontaneous autoantibody-mediated disease,
whereas high-fat LA-rich diets increase disease severity. In
experimentally induced T cell-mediated autoimmune disease, EFAD diets
or diets supplemented with long-chain n-3 PUFA augment disease,
whereas n-6 PUFA prevent or reduce the severity. In contrast, in both
T cell- and antibody-mediated autoimmune disease, the
desaturated/elongated metabolites of LA are protective. PUFA of both
the n-6 and n-3 families are clinically useful in human
autoimmune-inflammatory disorders, but the precise mechanisms by which
these fatty acids exert their clinical effects are not well
understood. Finally, the view that all n-6 PUFA are proinflammatory
requires revision, in part, and their essential regulatory and
developmental role in the immune system warrants appreciation.
PMID: 12848277 [PubMed - in process]
SEE!
This doesn't make sense for me! They haven't gotten this down in
the context of Th1 and Th2 versus Th0, have they?
> J.
JXStern
>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12848277&dopt=Abstract
>School of Chemical and Life Sciences, University of Greenwich at
>Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
>L.Ha...@gre.ac.uk
>
>has a demonstrable critical role in long-chain n-3 PUFA interactions
>with immune functions, often reversing the effects of fish oil.
> PUFA of both
>the n-6 and n-3 families are clinically useful in human
>autoimmune-inflammatory disorders, but the precise mechanisms by which
>these fatty acids exert their clinical effects are not well
>understood.
>Finally, the view that all n-6 PUFA are proinflammatory
>requires revision, in part, and their essential regulatory and
>developmental role in the immune system warrants appreciation.
>This doesn't make sense for me! They haven't gotten this down in
>the context of Th1 and Th2 versus Th0, have they?
Nope.
That last article is quite the laff-riot, shows just about where we
are in understanding any of this.
I think it comes down to eating a modest, balanced diet. Thank you,
ladies and germs.
J.
Randall
> On 18 Dec 2003 21:10:57 -0800, ranh...@aol.com (Randall) wrote:
> >http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12848277&dopt=Abstract
> >School of Chemical and Life Sciences, University of Greenwich at
> >Medway, Chatham Maritime, Kent ME4 4TB, United Kingdom.
> >L.Ha...@gre.ac.uk
> >
> > Vitamin E
> >has a demonstrable critical role in long-chain n-3 PUFA interactions
> >with immune functions, often reversing the effects of fish oil.
GulP! Don't swill to much vitamin E you E'ers out there!
> ...
> > PUFA of both
> >the n-6 and n-3 families are clinically useful in human
> >autoimmune-inflammatory disorders, but the precise mechanisms by which
> >these fatty acids exert their clinical effects are not well
> >understood.
This is a really big DUH! R-LOX and stereoconfigured R-HETE
elude me unless the LPS is driving that mechanism somehow
other then what i suspect already.
> ...
> >Finally, the view that all n-6 PUFA are proinflammatory
> >requires revision, in part, and their essential regulatory and
> >developmental role in the immune system warrants appreciation.
Nonsense. If your skewed to Th1 its all to true. I may have
been skewed to Th1 due to this funky freaking oil at an
eary age and my P genes of course.
Is this study a shill for the soy bean oil producers or what?
I may not like the added price of many goods due to trial attorneys.
But i'm now wondering what i could get for to many years
of p due to excess omega-6 disease?
> ...
> >This doesn't make sense for me! They haven't gotten this down in
> >the context of Th1 and Th2 versus Th0, have they?
>
> Nope.
>
> That last article is quite the laff-riot, shows just about where we
> are in understanding any of this.
A real quagmire alright.
My P patches of Plaque know the inflammatory reddish truths.
The part about vitamin E was a shocker. I stopped all not natural
vitamin E years ago and then only took the acetate natural E and then with
mixed tocopherols and finally couldn't see any difference in
anything related to P. The cheaPo vit. E's softgels had soy bean oil and
they actually did flare me. I wouldn't even take CoQ-10
in a soy bean base softgel as it would flare me.
I think i'm allergic to soybeans and their oils. Do they
have some peculiar lectins in them? I'll have to check.
Then again my FSO (flax seed oil) has some vitamin E
in it as a preservative. Also a spritz of rosemary oil
extract and ascorbyl palmitate to preserve the FSO prior
to consumption.
The rosemary oil reminds one of Ed Andersons adverse p
consequences to this phenol? I'll have to check that
one out as to IgG1/4 reactions someday.
I could find one without those particular preservatives
if i really felt a threat to my P well being.
>
> I think it comes down to eating a modest, balanced diet.
Easier said then done. And what about balanced
genes? You have to admit to the P DNA multifactorial
genes in this equation don't you?
JXStern
>The part about vitamin E was a shocker.
I try to avoid topical E, it feels nice but seems to irritate the
underlying inflammation. I suppose this is an unusual reaction on my
part. I am eating those DHA eggs with 10x the vitamin E. Oh well.
>I think i'm allergic to soybeans and their oils.
Seems entirely possible.
>You have to admit to the P DNA multifactorial
>genes in this equation don't you?
Of course, that and nothing else, is basically what I'm saying, at
least all the rest is commentary, symptom management, avoiding what
those genes makes us sensitive to that average people cope with
harmlessly.
J.
Izabela Dorota Grande
Psorisan, so a corp in Norway have. This cream is so far the best I have try
ever. And i amost good now. I recomand ewerybody to try this cream. I only
have the mailadress to this Corp.
har...@grande.as (Psorisan Cream)
Terje Hagen
Bergen/Norway
"skeatsan''co" <overt...@overthemoonagain.com> skrev i melding
news:5KgDb.59107$Y72....@news-lhr.blueyonder.co.uk...