Turmeric
Sad Man
http://www.floridatoday.com/!NEWSROOM/healthstoryA10174A.htm
....and wondered if anyone here has experimented with this spice.
If so, tell us your experience.
Is this something you would just buy a bottle of at the grocery store?
HH
ingesting even small amounts. It should be treated with caution.
Try a Google search "turmeric + allergic reactions" and you may be
surprised - it can be the cause of powerful reactions!
HH
----------------------------------------------------------------------------
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"Sad Man" <boyd...@msn.com> wrote in message
news:24acec0c.03101...@posting.google.com...
Jeff Mowatt
Indian sub-continent and also significant number in the UK. I reckon that
makes about a billion or so.
Strange thing is I haven't eaten much in recent months and my P has broken
out during this time.
It doesn't appeal to me as something to sprinkle on cereal, much better to
cook with it! Got an Indian restaurant near home?
Jeff
"Sad Man" <boyd...@msn.com> wrote in message
news:24acec0c.03101...@posting.google.com...
JXStern
>Is this something you would just buy a bottle of at the grocery store?
Yes, it is a common spice.
I've been taking a "liver formula" capsule of milk thistle, dandelion
root, and turmeric from Trader Joe's. I won't swear that these pills
do anything but I take them because I have the impression that they
help overall and make me less sensitive to food reactions that can
affect the state of my p.
Read the labels on any spicey foods you buy and consume, you're
probably getting at least a bit of it already!
J.
HH
"JXStern" <JXSternC...@gte.net> wrote in message
news:b7viovonn5kam228e...@4ax.com...> Read the labels on any
spicey foods you buy and consume, you're
> probably getting at least a bit of it already!
> J
-----------------------------
Couldn't agree more . . it's the little bits that cause me problems. Both
my wife and I are expert at reading the labels.
HH
Randall
> >Is this something you would just buy a bottle of at the grocery store?
>
> Yes, it is a common spice.
But, you need to beware. See below.
>
> I've been taking a "liver formula" capsule of milk thistle, dandelion
> root, and turmeric from Trader Joe's. I won't swear that these pills
> do anything but I take them because I have the impression that they
> help overall and make me less sensitive to food reactions that can
> affect the state of my p.
This sounds great. How much of each ingredient?
And whats the recommended dosages?
>
> Read the labels on any spicey foods you buy and consume, you're
> probably getting at least a bit of it already!
Some spices and herbs are good for P and some very common
ones may not be so good.
Why does the paganO diet nix peppers? Or is it spicy food he's
knocked out in general? And why?
There are spicy connections with NF-kappaB (NF-kB) and
TNF-alpha with turmeric (aka-curcumin) as pointed out
in the article by boydoe69.
Lets examine the NF-kB pathways.
http://www.biotechjournal.com/Pathways/nf-kb.htm
This next one is easier to read, (their trying to sell you something)
http://www.thaiwave.com/networkantioxidants/nfkb.htm
(click on the diagram to enlarge it)
Go forward or backward to see TNF or other ROS
agents. TNF induces NF-kB and if your overweight
your generating TNF from the white adipose tissue (fat).
That may be a huge factor in what levels of severity you
may be having with your psoriasis. Many severe folks
should be able to knock it down to mild, like myself
for instance.
A few more clicks on the next page and there are
some charts on ALA and glutathione which have been
speculated to help psoriasis as well as increase
quality of life if not length?
What is turmeric?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9134658&dopt=Abstract
The natural occurring pigment curcumin, a major component of the spice
tumeric, has been described to have antioxidative,
anti-tumorpromoting, anti-thrombotic and anti-inflammatory properties.
It appears, that the pleiotropic effects of curcumin are at least
partly due to inhibition of the transcription factors NF-kappa B and
AP-1.
[snip]
Thus, curcumin inhibits NF-kappa B and AP-1 by two different
mechanisms and reduces expression of endothelial genes controlled by
both transcription factors in vitro.
How much Turmeric does one get in the average curry powder?
Not enough!
What about the other ingredients?
NOt good!
Why?
The mix looks like this: Chilies, black pepper, curry leaves,
fenugreek,
ginger and other spices
Trying a curry supplement from a bonafide distributor may be the
best option if your serious about slowing p/PsA inflammation.
Curry/turmeric works to heal the liver cells. Silymarin from milk
thistle is
another good herb for the liver cells and will help lower psoraisis.
It may say so right here if there was an abstract there,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10468651&dopt=Abstract
For 671 abstracts on silymarin (milk thistle) go to www.pubmed.com
and enter: silymarin
Back to turmeric/curcumin,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12660143&dopt=Abstract
The characteristics of curcumin, including antioxidant potential,
reduction of activated HSC growth, and no adverse health effects, make
it a potential antifibrotic candidate for prevention and treatment of
hepatic fibrosis.
One of the hallmarks of my psoriasis is high liver enzymes indicating
ROS or LPS goofing up the proper functioning of the kupffer cells etc.
Is this one of those bad P genes? Could be. Its the chloride
co-transporter
gene thats at play in this scenario.
In order to stop psoriasis you must stop it in the gut where LPS gains
entrance due to mechanical problems, the liver where detox takes
place
and the skin where the visible manifestation reminds us that something
is
wrongO.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12473502&dopt=Abstract
Curry protects skin from sun rays.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12878172&dopt=Abstract
Inhibitors of the transcription factors AP-1 (nordihydroguaiaretic
acid, NDGA) and NF-kappaB (curcumin, proteasome inhibitors, and
Bay-11-7085) suppressed TNF-alpha-induced MMP-13 expression in primary
chondrocytes and SW1353 cells.
(NDGA, hey thats the creosote bush, the longest lived plant
in the world, IIRC. Beware of using it due to possible carcinogens)
Slowing down TNF-alpha is good as that slows NF-kB (nf-kappaB).
If you smoke cigarettes and drink alcohol, curry/turmeric (curcumin)
should
be your friend. (I'd try the pills even if you love curry foods)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12807725&dopt=Abstract
The signal transduction pathway that mediates the effects of CS is not
well understood but nuclear factor-kappa B (NF-kappaB) is probably
involved.
[snip]
Overall our results indicate that CS-induced NF-kappaB activation and
NF-kappaB-regulated gene expression in human non-small cell lung
carcinoma cells is suppressed by curcumin through suppression of
IkappaBalpha kinase.
Remember that the percentage of psoriatics that smoke and drink is
high. lol
Why are psoriatics so faustian? Just lucky on the addictive brain
cells i
guess? It may even be a factor in our P multi-factorial genes to a
small,
but important extent.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12388178&dopt=Abstract
Induction of NF-kappaB-mediated gene expression has been implicated in
the pathogenesis of alcoholic liver disease (ALD). Curcumin, a
phenolic antioxidant, inhibits the activation of NF-kappaB.
So, if you do get tiPPsy once in awhile. Curry/curcumin pills may be
a saving grace for liver/skin/brain/gut cells.
But, i'd suggest you tiP the green tea instead. Camellia senses is
green tea and helps with p in many ways.
Spice up your P life (BUT-avoid the black peppers, or at least try to)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12067569&dopt=Abstract
A wide variety of phenolic substances derived from spice possess
potent antimutagenic and anticarcinogenic activities. Examples are
curcumin, a yellow colouring agent, contained in turmeric (Curcuma
longa L., Zingiberaceae), [6]-gingerol, a pungent ingredient present
in ginger (Zingiber officinale Roscoe, Zingiberaceae) and capsaicin, a
principal pungent principle of hot chili pepper (Capsicum annuum L,
Solanaceae). The chemopreventive effects exerted by these
phytochemicals are often associated with their antioxidative and
anti-inflammatory activities. Cyclo-oxygenase-2 (COX-2) has been
recognized as a molecular target of many chemopreventive as well as
anti-inflammatory agents. Recent studies have shown that COX-2 is
regulated by the eukaryotic transcription factor NF-kappaB. This short
review summarizes the molecular mechanisms underlying chemopreventive
effects of the aforementioned spice ingredients in terms of their
effects on intracellular signaling cascades, particularly those
involving NF-kappaB and mitogen-activated protein kinases.
I believe that the peppers (piperines) upregulate cell permeability
and thats not
so good for psoriasis, due to increased LPS absorption from the gut,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12046863&dopt=Abstract
Piperine (1-Piperoyl piperidine) is a major alkaloid of Piper nigrum
Linn. and Piper longum Linn. It is shown to possess
bioavailability-enhancing activity with various structurally and
therapeutically diverse drugs. The mechanism of enhancing the
bioavailability, is, however, not understood. We hypothesize that
piperine's bioavailability-enhancing property may be attributed to
increased absorption, which may be due to alteration in membrane lipid
dynamics and change in the conformation of enzymes in the intestine.
What is piperine?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9536651&dopt=Abstract
Piperine, [1-[5-[1,3-benzodioxol-5-yl]-1-oxo-2,4, pentadienyl]
piperidine], is a pungent alkaloid present in Piper nigrum Linn, and
P. longum Linn. [snip] It may modulate membrane dynamics due to its
easy partitioning thus helping in efficient permeability across the
barriers.
(note- piper nigrum is black pepper! Now recall the curry ingredients
up above.
Black pepper is #2. So, any old curry powder should be ruled out, if
it
has high levels of black pepper.)
My feeling on it is, it allows more LPS into
the cell/system. Go back and look at the diagram in the first link.
There's some
LPS sitting on the cell membrane looking for entry to cause its
mischief.
LPS->CD14->NF-kB activation. IIRC (there may be some TLR-4 also)
Why isn't LPS detoxed in the liver? Keyword: chloride co-transporter
gene
(and search in the psoriasis newsgroup only) you could
do it this way www.deja.com (keyword) psoriasis chloride
co-transporter
My whole attack on psoriasis is in blocking translocation of LPS from
the gut into the system. Thus draining inflammatory fuel from the
psoriasis equation. IMO
Its the food way to less P. And what do you think those cell
membranes,
that each and every cell in your body is contained in are made out of?
Fats and lipids. And they aren't all equal. Search on omega3's and 6's
to try to close up those leaky little membranes. lol
For this one, suffice it to say, try to avoid the vegetable oils.
If you wish to find some links, keyword: cd14 LPS and or tlr4
For the oils, just check the psoriasis newsgroup for omega3.
There are other herbs also,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11999122&dopt=Abstract
A large number of compounds are currently known as NF-kappaB
modulators and include the isoprenoids, most notably kaurene
diterpenoids and members of the sesquiterpene lactones class, several
phenolics including curcumin and flavonoids such as silybin.
This last one is the active compound in milk thistle/silymarin etc.
Here's a whole thread on silymarin/silybum,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=12967193
What does this weed/herb look like?
http://tncweeds.ucdavis.edu/photos/silma01.jpg
Or you could try JSterns trader joe's liver formula,
that also contains dandelion.
A really great idea would be to use silymarin and curcumin at the
same time. Also ALA and NAC for those life extender types.
Toss in some green tea pills and yahoo. Go for it.
Please let us know if you do!
Caveat emptor on turmeric and curcumin,
http://www.itmonline.org/arts/turmeri3.htm
What it looks like,
http://www.itmonline.org/arts/turmeri3.htm#figure 3
StoPPing lps is a good thing,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11747626&dopt=Abstract
Lipopolysaccharide (LPS) is a bacterial cell component that plays
multifunctional roles in inflammatory reactions, and one of the roles
is as a powerful stimulator of bone resorption. LPS stimulated bone
resorption via CD14 in mouse calvaria and was reported to function as
a receptor for bacterial LPS complexed with serum proteins.
Whats the cause of P?
It may be a bunch of things. As a bunch of herbs/weeds, helps all
those pathways.
Yet, LPS and a Th1 profile lead the list for me.
>
> J.
JXStern
>This sounds great. How much of each ingredient?
>And whats the recommended dosages?
milk thistle fruit, powdered extract 30:1 (silybum marianum) 250mg**
yielding 80% silymarin (200mg). dandelion root, powdered (taraxacum
officinale) 55mg** turmeric rhizome, powdered (curcuma longa l.)
27.5mg**
** Daily value not established.
Serving size one capsule.
Suggested use 1 capsule 3-6 times daily or as directed by a health
practitioner, keep out of reach of children.
I've been taking one AM and one PM, generally, fwiw.
J.
evetsm
psoriasis
-----------------------------------------------------------------------
Curcumin inhibits Th1 cytokine profile in CD4+ T cells by suppressing
interleukin-12 production in macrophages.
Kang BY, Song YJ, Kim KM, Choe YK, Hwang SY, Kim TS.
College of Pharmacy, Chonnam National University, Kwangju 500-757,
South Korea.
1 Interleukin-12 (IL-12) plays a central role in the immune system by
driving the immune response towards T helper 1 (Th1) type responses
which are characterized by high IFN-gamma and low IL-4 production. In
this study we investigated the effects of curcumin, a natural product
of plants obtained from Curcuma longa (turmeric), on IL-12 production
by mouse splenic macrophages and the subsequent ability of these cells
to regulate cytokine production by CD4+ T cells. 2 Pretreatment with
curcumin significantly inhibited IL-12 production by macrophages
stimulated with either lipopolysaccharide (LPS) or head-killed
Listeria monocytogenes (HKL). 3 Curcumin-pretreated macrophages
reduced their ability to induce IFN-gamma and increased the ability to
induce IL-4 in Ag-primed CD4+ T cells. Addition of recombinant IL-12
to cultures of curcumin-pretreated macrophages and CD4+ T cells
restored IFN-gamma production in CD4+ T cells. 4 The in vivo
administration of curcumin resulted in the inhibition of IL-12
production by macrophages stimulated in vitro with either LPS or HKL,
leading to the inhibition of Th1 cytokine profile (decreased IFN-gamma
and increased IL-4 production) in CD4+ T cells. 5 These findings
suggest that curcumin may inhibit Th1 cytokine profile in CD4+ T cells
by suppressing IL-12 production in macrophages, and points to a
possible therapeutic use of curcumin in the Th1-mediated immune
diseases.
Randall
Hey, i said post the link, (you didn't have the date or PMID#)
OTOH, good work! But, will JStern flip-floP big time on a P flare if
he stops his curcumin/trader Joe's supplements?
And with winter coming will it be worst and how would
we even know? We need 100 J's. lol Get the clone machine out.
Thanks again for this one,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10510448&dopt=Abstract
Ok, i made a mistake in the TLR for P yesterday, i said TLR4 and its
not known for P. Yet.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10510448&dopt=Abstract
I figured that it had to be TLR4 due to LPS affinity. Wrong again. :(
I think it was the Oct./2001 abstract that threw me. Its number
8 or 11 in the thread above.
Here are the TLRs,
http://www.biotechjournal.com/Pathways/tollvol2.htm
This one may give a few more hints,
http://rex.nci.nih.gov/RESEARCH/basic/eib/ds18.gif
It comes from here,
http://rex.nci.nih.gov/RESEARCH/basic/eib/segal.htm
Eureka! I just found this science news page,
http://www.sciencenews.org/20010908/bob9.asp
We may as well show the TNF signaling also,
http://www.biotechjournal.com/Pathways/tnf.htm
I found a 100 cap bottle of turmeric, 720mg's per cap, for
$4.49.
Since J and I are already P clones, i may as well be on
curcuminoids at this price. What a spice!
Now, if it only does something. What did the boydoe article say,
the guy used it on his breakfast food?
Cheerio's or Cap'N Crunch?
JXStern
>OTOH, good work! But, will JStern flip-floP big time on a P flare if
>he stops his curcumin/trader Joe's supplements?
No, doesn't seem to. But then, it doesn't seem to help much directly,
either. Just the entire liver thing seems to make me less sensitive
to food generally. But then #2, so does the grapefruit juice I'm
still drinking, and that much more dramatically.
J.
evetsm
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.03101...@posting.google.com>...
>
>
> Hey, i said post the link, (you didn't have the date or PMID#)
Sorry.
Better to go to an Indian store and buy turmeric by the packet, take
it by the teaspoon. Dirt cheap stuff. Powerful antioxidant.
Sad Man
$4.49."
Where at?
Randall
> "I found a 100 cap bottle of turmeric, 720mg's per cap, for
> $4.49."
Also says 2 caps, 2-3 X's a day.
6 caps a day is over 4 grams/day.
A gram looks like about a quarter of a teaspoon, iirc.
No wonder that guy in your article was sPooning it on his
cereal. A teaspoon or so would be 4-8 grams (level -to- heaping).
>
>
> Where at?
Go to www.swansonvitamins.com
Or call them at 800 437 4148
I have a catalogue that says the price is good till Nov. 29,
2003.
You may need a code#. If your a first time orderer i
doubt it.
Evetsm may have the best idea. Try a local middle/far eastern
grocery and see if you can buy it in bulk. The brand
that i quoted the ingredients from previously is Sadaf
and 4oz (113grams) was less then $2.00 (US).
They may have pure Turmeric in their product line, for all
i know. I'm gonna ask the grocer if he can show
me their line of products to determine that. I'll try
a google on it also. :)
Randall
>
> Ok, i made a mistake in the TLR for P yesterday, i said TLR4 and its
> not known for P. Yet.
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10510448&dopt=Abstract
What's this? Its that one from above that evetsm posted.
I posted it by mistake. Mea culPa :(
Here's what i meant to post. My keywords are a little different
so number 8 or 11 isn't right either.
A thread on TLRs. Starting with a current one that has
keyword: psoriasis
Maybe i used Tlr2 with psoriasis in the one i did
yesterday?
I'll try that also, next.
>
> I figured that it had to be TLR4 due to LPS affinity. Wrong again. :(
> I think it was the Oct./2001 abstract that threw me. Its number
> 8 or 11 in the thread above.
The date would still be right. :)
In essence i'm trying to build the case that LPS
enters the cells thru TLR4 receptors and the P mayhem
reigns on. Its an area that isn't clear yet and when it
is, so will we P's be. :)
Last week i noticed that one of the nobel prize winners
was for the structure of these pores in the cell membranes.
I can find the info for anyone whose interested.
>
> Here are the TLRs,
> http://www.biotechjournal.com/Pathways/tollvol2.htm
This shows the TLR's and what pathogen enters the cells.
Or was that the next one?
>
> This one may give a few more hints,
> http://rex.nci.nih.gov/RESEARCH/basic/eib/ds18.gif
> It comes from here,
> http://rex.nci.nih.gov/RESEARCH/basic/eib/segal.htm
I just love these haPPy smiling TLR researchers.
Go you happy team of scientists! Figure this stuff out!
RA! Ra! Sisk boom Bah! or is that Rah rah? But the suns cool too!
>
> Eureka! I just found this science news page,
> http://www.sciencenews.org/20010908/bob9.asp
This is great for learning this stuff. The first quarter
of it is right on, i'm excited to finish it and go back
and LOOK at those TLR links. Just remember that those
illustrations are of extracellular (outside the cell),
the cell membrane (where the TLRs are) and intracellular
(inside the cells).
SEE! How easy it is to learn this?
>
> We may as well show the TNF signaling also,
> http://www.biotechjournal.com/Pathways/tnf.htm
This TNF pathway is the basis for all the current croP
of biologic drugs. Their designed to block a bunch of it.
Not all of it! As you would be exposed to an even worse fate
then P. Like C for instance. As in cancer.
TNF-alpha (TNF) continually knocks C's block off day in and
day out. Every now and then a cell's DNA goes awry and
the TNF may not be there to stop the C from develoPing
into a major life threatening disease.
For this reason, being TH1 skewed and having to much
TNF in our poor little p bodies is a good and bad thing.
We want the level that is just right. And its up to
you and your doctor to work to-gether to achieve
that. All based on good science and a little healing
arts on your derms part.
Here is the MAPk pathway, ( a great learning tool)
http://www.biocreations.com/animations/_portfolio/MAPK.html
Click this on and click start and next till you see the end.
It came from here,
http://www.geocities.com/mesentsev/ma_recherche.html
And is linked under "On-line Resources": Animated Version
of p42/p42 MAPK cascade (link to BioCreatures Web site)
What is this MapK pathway?
Mitogen-Activated Protein Kinase Cascade (MapK)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14553829&dopt=Abstract
The role of p38 mitogen-activated protein kinase (MAPK) activation in
lipopolysaccharide (LPS)-induced myocardial dysfunction has not been
clearly defined.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535196&dopt=Abstract
Jan/2003
Bone morphogenetic proteins (BMP) are members of the transforming
growth factor-beta superfamily regulating a large variety of biologic
responses in many different cells and tissues during embryonic
development and postnatal life. BMP exert their biologic effects via
binding to two types of serine/threonine kinase BMP receptors,
activation of which leads to phosphorylation and translocation into
the nucleus of intracellular signaling molecules, including Smad1,
Smad5, and Smad8 ("canonical" BMP signaling pathway). BMP effects are
also mediated by activation of the mitogen-activated protein (MAP)
kinase pathway ("noncanonical" BMP Signaling pathway). BMP activity is
regulated by diffusible BMP antagonists that prevent BMP interactions
with BMP receptors thus modulating BMP effects in tissues. During skin
development, BMPs its receptors and antagonists show stringent
spatiotemporal expressions patterns to achieve proper regulation of
cell proliferation and differentiation in the epidermis and in the
hair follicle. In normal postnatal skin, BMP are involved in the
control of epidermal homeostasis, hair follicle growth, and
melanogenesis. Furthermore, BMP are implicated in a variety of
pathobiologic processes in skin, including wound healing, psoriasis,
and carcinogenesis. Therefore, BMPs represent new important players in
the molecular network regulating homeostasis in normal and diseased
skin. Pharmacologic modulation of BMP signaling may be used as a new
approach for managing skin and hair disorders.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12507899&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12413764&dopt=Abstract
Psoriatic skin shows markedly increased keratinocyte proliferation and
altered differentiation with various abnormal signalling pathways. In
the present study, we investigated the expression of mitogen-activated
protein kinases in psoriatic skin. Immunohistochemical study showed
increased extracellular regulated kinase (ERK) and c-Jun N-terminal
kinase (JNK) expression in the nuclei of involved epidermis. Western
blot analyses confirmed the increased active phospho-ERK and
phospho-JNK expression in the involved epidermis. In contrast,
expression pattern of p38 was not different between the involved and
uninvolved epidermis, which was confirmed by western blot analysis.
These results indicate that psoriatic epidermis shows selective
activation of ERK and JNK, which might be related to
hyperproliferation and abnormal differentiation of psoriatic
epidermis. Copyright 2002 Elsevier Science Ireland Ltd.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10836611&dopt=Abstract
Keratinocytes of inflamed epidermis (psoriasis, wound healing) are
hyperproliferative and display an abnormal differentiation programme.
This regenerative differentiation pathway is characterized by the
induction of genes that are not expressed by keratinocytes in normal
skin, such as the cytokeratins CK6, CK16, CK17, and the proteinase
inhibitor SKALP/elafin. In the study reported here we investigated the
induction and regulation of SKALP expression as a marker for
regenerative differentiation in epidermal keratinocytes. Various
cytokines and growth factors known to be present in psoriatic
epidermis were examined for their ability to induce SKALP gene
expression in cultured human keratinocytes. Tumour necrosis
factor-alpha (TNF-alpha) and serum were found to be potent inducers of
SKALP expression at both the mRNA and the protein levels. SB202190 or
SB203580, two specific p38 MAP kinase inhibitors almost completely
blocked the induction of SKALP expression by TNF-alpha and serum.
These results suggest that in keratinocytes, p38 activity is crucial
for the induction of SKALP gene expression. These findings could be
relevant for the elucidation of the mechanisms involved in normal and
disturbed epidermal differentiation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7635978&dopt=Abstract
Previous studies from other laboratories suggest that linoleic acid
and its metabolites, hydroperoxyoctadecadienoic acids, play an
important role in modulating the growth of some cells. A correlation
has been demonstrated between hydroperoxyoctadecadienoic acids and
conditions characterized by abnormal cell growth such as
atherosclerosis and psoriasis. To determine if linoleic acid and its
metabolites modulate cell growth in atherosclerosis, we measured DNA
synthesis, protooncogene mRNA expression, and mitogen-activated
protein kinase (MAPK) activation in vascular smooth muscle cells
(VSMC). Linoleic acid induces DNA synthesis, c-fos, c-jun, and c-myc
mRNA expression and MAPK activation in VSMC. Furthermore,
nordihydroguaiaretic acid, a potent inhibitor of the lipoxygenase
system, significantly reduced the growth-response effects of linoleic
acid in VSMC, suggesting that conversion of linoleic acid to
hydroperoxyoctadecadienoic acids (HPODEs) is required for these
effects. HPODEs also caused significant induction of DNA synthesis,
protooncogene mRNA expression, and MAPK activation in growth-arrested
VSMC, suggesting that linoleic acid and its metabolic products,
HPODEs, are potential mitogens in VSMC, and that conditions such as
oxidative stress and lipid peroxidation which provoke the production
of these substances may alter VSMC growth.
PMID: 7635978 [PubMed - indexed for MEDLINE]
Well, i know Kim can enjoy this!
Then again, we'd all love to forget the whole darn P
experience. CePt for,
Evetsm could make some TH1/2 hay with a CLA
psoriasis newsgroup search. Showing his PPAR & P
considerations. <G>
And does turmeric work better for a Th1 skewed person
who takes CLA or not? That has P of course! Th2 doesn't count. lol
>
evetsm
>
> Go you happy team of scientists! Figure this stuff out!
Bag of laughs , researching this stuff. I knew it.
TH2 have a real problem with cancer risk and there are studies
suggesting this, one small consolation for psoriatics. No bag of
laughs.
While GLA seems to suppress TH2 it also reduces TNF, useful in
psoriasis perhaps , which fits with J. reporting some improvement ,
and AA metabolites may actually help psoriasis while linoleic is
probably detrimental according to the study you cited. Is this a small
hint at low carb for psoriasis? AA-meat, linoleic-vegetable. In any
case, none of the studies are unequivocal.
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(good for
psoriasis?). 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.
JXStern
>While GLA seems to suppress TH2 it also reduces TNF, useful in
>psoriasis perhaps , which fits with J. reporting some improvement ,
Really? Hmph.
I've actually cut down my EPO usage by about 90% since switching to
the grapefruit juice and/or DHA-enriched eggs (and also the liver
formula with milk thistle and turmeric). The benefits I took EPO for
were first, 90% reduction of scratch/bleed, and second, keeping the
nails clear. With the juice and/or eggs, the scratch/bleed is down
99%, and the nails have stayed clear over a year, with much less EPO
than was required for this before, and I suspect zero would be OK as
well.
Maybe I should crank it up again from this new base and see if
anything happens.
You want another anecdotal dietary point, I suspect that nuts
facilitate new plaques/spots on me, especially cashews and/or pecans.
J.
Sad Man
Hey, howsabout a pound of the stuff for under six bucks? While
surfing I found this site. http://www.spicebarn.com/turmeric.htm
I found if look at places selling bulk "cooking" spices, it ends up
being much cheaper than bulk health products. Thing is, I guess you
don't really know what you're getting without the standardizations?
Randall
> ranh...@aol.com (Randall) wrote in message news:<df7e2c67.03101...@posting.google.com>...
> > boyd...@msn.com (Sad Man) wrote in message news:<24acec0c.03101...@posting.google.com>...
> Hey, howsabout a pound of the stuff for under six bucks? While
> surfing I found this site. http://www.spicebarn.com/turmeric.htm
> I found if look at places selling bulk "cooking" spices, it ends up
> being much cheaper than bulk health products. Thing is, I guess you
> don't really know what you're getting without the standardizations?
Hey, thanks for the link!
I found a 7oz (198grams) plastic bottle for $1.99
at my local middle eastern store. Sure enough it was
the Sadaf brand. Go to www.sadaf.com and enter turmeric
in the search box and bingo.
I used curry powder and a few teaspoons turmeric in my
curry today. Fried up some red/green peppers and onions
with garlic and added the curry/turmeric to the hot
olive oil and put in some left over meat with left over
rice and had a delicious meal. I do use kimbo
fish sauce to tie it to-gether and add chopped
parsley in the last few minutes. Other options would
be mint, cilantro, japalenos, fish, poultry, and coconut
milk/butter to thicken.
Whoops, i had fresh basil also. A good combo for lamb
may be Rosemary, thyme and sage. And different veggies
you happen to like.
Then again you may have some good breakfast food that
needs spicing uP.
Randall
> > I just love these haPPy smiling TLR researchers.
> >
> > Go you happy team of scientists! Figure this stuff out!
>
>
> Bag of laughs , researching this stuff. I knew it.
First things first may be the route to the prize.
>
>
> TH2 have a real problem with cancer risk and there are studies
> suggesting this, one small consolation for psoriatics. No bag of
> laughs.
Fixing the master hormone rather then tweaking here and
there seems most logical.
>
>
>
> While GLA seems to suppress TH2 it also reduces TNF, useful in
> psoriasis perhaps , which fits with J. reporting some improvement ,
> and AA metabolites may actually help psoriasis while linoleic is
> probably detrimental according to the study you cited. Is this a small
> hint at low carb for psoriasis? AA-meat, linoleic-vegetable. In any
> case, none of the studies are unequivocal.
I'm headed towards the leptin angle now.
Since TGF-beta is tied to leptin and downregulated in psoriasis,
adjusting leptin may help P,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11192627&dopt=Abstract
Leptin signals through the Ob receptor, which is closely related to
the gp130 cytokine receptor. Here we show that leptin can induce
expression of the neuropeptide gene vasoactive intestinal peptide
(VIP) through the VIP cytokine response element, the same element that
mediates the response to the gp130 cytokines. Leptin acts
synergistically with TGF-beta to activate transcription through this
element.
Wouldn't that skew the Th1 back to Th2?
First deal with leptin and insulin resistance and the TNF,
NF-kappaB fall back into normal ranges. I hoPe!
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14527734&dopt=Abstract
Transforming growth factor beta (TGFbetas) have a major
antiproliferative action in epidermis. [snip]
The present investigation strongly suggest that the TGFbeta signaling
pathway is downregulated in psoriatic skin and this situation leads to
abnormal cell proliferation due to a functional decrease in growth
regulation.
>
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12848277&dopt=Abstract
This is a good one. But researchers aren't thinking of the
master hormone leptin in relationship to TH situations yet.
Untill resistance is dealt with the inflammatory pathways
won't budge and whatever way your skewed will remain till
kingdom come.
What do you think?
>
> 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(good for
> psoriasis?).
But only works well now based on injections. Sorta takes the
tactile gastronomical pleasure out of eating.
>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 this throws me. JStern does well with n-6 and it flares
me. Using the high DHA eggs i can muddle by a bit without
to much problem. Would the CLA make a big difference?
I need to check the abstracts on that one. Can you
check it with leptin?
TIA
JXStern
>And this throws me. JStern does well with n-6 and it flares
>me.
Not just any n-6 but GLA (EPO).
And on my present diet, the EPO seems to encourage a bit of extra
inflammation after a few days.
Something in the grapefruit, or eggs, or (another factor I'm playing
with) cruciferous veggies, (and/or the milk thistle/tumeric and/or
Q10) may restore my natural GLA metabolism. At the same time it seems
I can eat beef (n-6, AA) with only the most minor flaring ... until
the gout steps in, perhaps, another country heard from.
Fun and games all over.
J.
Randall
> On 16 Oct 2003 17:40:13 -0700, ranh...@aol.com (Randall) wrote:
> >And this throws me. JStern does well with n-6 and it flares
> >me.
>
> Not just any n-6 but GLA (EPO).
Yes, thats nice. A little info for those newbies,
http://www.fatsforhealth.com/library/libitems/borage_oil.php
Once linoleic acid is ingested it is acted upon by an enzyme called
Delta-6-Desaturase (D6D) which biochemically converts LA into GLA.
This is how we normally get our daily fix of GLA. Note the importance
of the enzyme D6D, without it we would be deficient in GLA no matter
how much linoleic acid we got in our diets. GLA is further converted
via a sequence of biochemical steps into a very important compound
called prostaglandin 1 (PG1) which is a key molecule for maintaining
healthy skin. PG1 exhibits a potent anti-inflammatory effect on the
skin and also is very effective in regulating water loss and
protecting the skin from injury and damage.2
The D6D enzyme is often referred to as a "lazy" enzyme. That is to
say, it can be slow in doing its job, and under some conditions may
actually be impaired. People with skin disorders such as eczema,
atopic dermatitis and psoriasis show increased levels of linoleic acid
with a simultaneous decrease in gamma linolenic acid.3 This evidence
strongly suggests a reduction in the activity of the D6D enzyme. And
as a consequence the resulting decrease in the synthesis of PGI may be
responsible for the characteristic dry skin and trans-epidermal water
loss observed in these people. It is here that the importance of
borage oil with its rich source of gamma linolenic acid becomes
evident. Used as a dietary supplement or even applied topically borage
oil can circumvent a "lazy" or impaired D6D enzyme by supplying the
body directly with GLA, thus allowing the production of normal levels
of PG1.
Wouldn't borage be cheaper then epo?
http://www.fatsforhealth.com/library/libitems/omega6.php
>
> And on my present diet, the EPO seems to encourage a bit of extra
> inflammation after a few days.
Something must be amiss with your D5D?
Lets see what i've said on it,
How many times i've brought up D6D or D5D,
http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=d6d+d5d&btnG=Google+Search&meta=group%3Dalt.support.skin-diseases.psoriasis
And D5D makes PGE2, so how many times on it?
http://groups.google.com/groups?hl=en&lr=&ie=ISO-8859-1&q=+PGE2&btnG=Google+Search&meta=group%3Dalt.support.skin-diseases.psoriasis
PGE2 doesn't stop till the white blood cells make PGE1.
Sounds simple doesn't it?
It means cutting out the refined carbs (sugars), some GTF
chromium with your borage/EPO, nicotinic acid, omega3 fats
etc.
Right now i'm on a CLA/leptin quest for these pathways.
Previously i may have eaten correctly but undone it with
loss of leptin resistance due to refined carbs eaten
at less then opportune mooments.
>
> Something in the grapefruit,
I'd say so and i'm sure its not just me.
Then again the canary in the P cave does sing a little louder.
>or eggs,
I'm hooked on the DHA/Omega-3 eggs from Gold Circle Farms.
Thanks again for this one.
I'm eating them guilt free for the first time in years.
>or (another factor I'm playing
> with) cruciferous veggies,
I haven't seen the sprouted broccoli supplement anywhere.
Remember how they touted the super duper levels of sulforaphane
in them? The effects are positive but short lived and you
need to consume them every day for maximum help with
cooling inflammation.
>(and/or the milk thistle/tumeric and/or
> Q10) may restore my natural GLA metabolism.
I'm looking more to leptin effects to correct metabolism
overall now. Cla again for this pathway. Tonalin
seems to be alot cheaper now that the cancer crowd
has cooled their jets on it.
I've started that massive over 50 down hill slide and
any extra sPare tire around the middle is certainly not warranted.
For less TNF-alpha, NF-kappaB, resistances of insulin and
leptin, one must lower white fat cells. The adiPose
cells must go with out question. They are an inflammatory organ
between you and your skin! Flax may have beneficial levels
of omega3/6, but the fat is overriding the good news
by pumping out the PGE2's into the P equation.
>At the same time it seems
> I can eat beef (n-6, AA) with only the most minor flaring ...
I've never had AA problems with beef either. Its been
the soy bean oils (veggie oils in general), grain fed
chicken eggs (regular eggs), and pork in this department.
>until
> the gout steps in,
And stePPing lively hurts and prevents exercise. Taking one
further down inflammatory pathways better not stepped in.
>perhaps, another country heard from.
You want to join me in nirvana? How about P free
island?
>
> Fun and games all over.
Right! Back to serious considerations and how do
we raise exercise and proper dietary rules to correct
good health and slow psoriasis. You might want to master
your leptin.
>
> J.
JXStern
>Wouldn't borage be cheaper then epo?
>http://www.fatsforhealth.com/library/libitems/omega6.php
Aren't there some questions of nasties in the borage? Anywho, the EPO
is mondo cheap at TJ's.
>> And on my present diet, the EPO seems to encourage a bit of extra
>> inflammation after a few days.
>
>Something must be amiss with your D5D?
Well it would be the n-6, as you say, if I already have enuf.
>Sounds simple doesn't it?
>It means cutting out the refined carbs (sugars), some GTF
>chromium with your borage/EPO, nicotinic acid, omega3 fats
>etc.
With the cruciferous, I seem to even get by with less of my main
source of n-3, the pickled herring snax.
>Right now i'm on a CLA/leptin quest for these pathways.
>
>Previously i may have eaten correctly but undone it with
>loss of leptin resistance due to refined carbs eaten
>at less then opportune mooments.
I don't know. When I've tried to cut the carbs, simple or complex, my
body just doesn't like it, I have the cravings, I get tired, and worst
of all, for the couple of weeks I've been able to maintain, I've seen
no benefits. I'm lower carb now than ten years ago, but it ain't no
Atkins diet I'm on.
I haven't followed all your leptin links, not sure just what the
theory going on here is, triggering antigens like LPS or metabolic
balancers or wot?
>>or eggs,
>
>I'm hooked on the DHA/Omega-3 eggs from Gold Circle Farms.
>Thanks again for this one.
>
>I'm eating them guilt free for the first time in years.
Do you associate any change in your p with the eggs?
And, are you also eating any significant amount of cruciferous
veggies, cole slaw, broccoli, whatever?
>>or (another factor I'm playing
>> with) cruciferous veggies,
>
>I haven't seen the sprouted broccoli supplement anywhere.
>Remember how they touted the super duper levels of sulforaphane
>in them? The effects are positive but short lived and you
>need to consume them every day for maximum help with
>cooling inflammation.
For me, the effect seems to last longer than the eggs. Without the
crux, I pretty much have to eat one small egg per day, or my skin
clearly misses it. With the crux, I seem to be able to go a couple of
days without the egg and without more slaw. Geez, trying to figure
this stuff out at the dietary level with one (1) patient, is like
trying to thread a needle while wearing mittens. In the dark. But
hey, it passes the time.
>I've started that massive over 50 down hill slide and
>any extra sPare tire around the middle is certainly not warranted.
>For less TNF-alpha, NF-kappaB, resistances of insulin and
>leptin, one must lower white fat cells. The adiPose
>cells must go with out question. They are an inflammatory organ
>between you and your skin!
I keep saying that, that I should try losing twenty pounds (which I
don't especially need to lose otherwise), before throwing myself onto
the needle for one of the biologics. Think I'll have another danish
and think about it some more.
>Flax may have beneficial levels
>of omega3/6, but the fat is overriding the good news
>by pumping out the PGE2's into the P equation.
Just keeping the n-3/n-6 balance, seems to be something my body isn't
very good at. Maybe nobody's is, but it doesn't matter so much if your
skin is in better shape, I dunno.
>>At the same time it seems
>> I can eat beef (n-6, AA) with only the most minor flaring ...
>
>I've never had AA problems with beef either. Its been
>the soy bean oils (veggie oils in general), grain fed
>chicken eggs (regular eggs), and pork in this department.
I've had minor reactions to beef before. I did try some ham recently
and had a minor flare, even through all the other stuff. Just a sign
I should keep kosher, I suppose.
>Right! Back to serious considerations and how do
>we raise exercise and proper dietary rules to correct
>good health and slow psoriasis. You might want to master
>your leptin.
I just don't grok this leptin stuff. I thought leptin is a class,
like cytokines, and there are good ones and bad ones, yet half these
articles just talk about "leptin". And our bodies create leptin(s),
and they are also dietary. I see a bunch of messages between you and
evetsm on it, but can't sort through them. You want to maybe start a
leptin thread to review your basic thoughts on the matter, I promise
to pay it more attention.
J.
Randall
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.03101...@posting.google.com>...
> > ranh...@aol.com (Randall) wrote in message
snip
>
> Fixing the master hormone rather then tweaking here and
> there seems most logical.
snip
>
> I'm headed towards the leptin angle now.
>
> Since TGF-beta is tied to leptin and downregulated in psoriasis,
> adjusting leptin may help P,
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11192627&dopt=Abstract
> Leptin signals through the Ob receptor, which is closely related to
> the gp130 cytokine receptor. Here we show that leptin can induce
> expression of the neuropeptide gene vasoactive intestinal peptide
> (VIP) through the VIP cytokine response element, the same element that
> mediates the response to the gp130 cytokines. Leptin acts
> synergistically with TGF-beta to activate transcription through this
> element.
>
> Wouldn't that skew the Th1 back to Th2?
> First deal with leptin and insulin resistance and the TNF,
> NF-kappaB fall back into normal ranges. I hoPe!
>
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14527734&dopt=Abstract
> Transforming growth factor beta (TGFbetas) have a major
> antiproliferative action in epidermis. [snip]
> The present investigation strongly suggest that the TGFbeta signaling
> pathway is downregulated in psoriatic skin and this situation leads to
> abnormal cell proliferation due to a functional decrease in growth
> regulation.
> >
> >
> > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12848277&dopt=Abstract
> Untill resistance is dealt with the inflammatory pathways
> won't budge and whatever way your skewed will remain till
> kingdom come.
snip
> I need to check the abstracts on that one. Can you
> check it with leptin?
>
> TIA
I went and got something already,
we can use cla to help balance leptin. Once you lose the weight you
may not need it.
And as a note, isn't the CLA levels higher in animals grazed on fresh
sprouted
grass? ANS. Yes!
You can buy this expensive grass ged beef on some web sites. Butt, why
bother?
A supplemental dose (a few grams a day) can be purchased
at the local health food store for the price of one steak.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12514304&dopt=Abstract
Isomers of conjugated linoleic acid (CLA) are found in beef, lamb and
dairy products. Diets containing CLA reduce adipose mass in various
depots of experimental animals. In addition, CLA delays the onset of
diabetes in the ZDF rat model for obesity-linked type 2 diabetes
mellitus. We hypothesize that there would be an inverse association of
CLA with body weight and serum leptin in subjects with type 2 diabetes
mellitus.
[snip]
Future studies are needed to determine a causal relationship, if any,
of t10c12-CLA or c9t11-CLA to modulate body weight and composition in
subjects with type 2 diabetes. Furthermore, determining the ability of
CLA isomers to influence glucose and lipid metabolism as well as
markers of insulin sensitivity is imperative to understanding the role
of CLA to aid in the management of type 2 diabetes and other related
conditions of insulin resistance.
Fixing lipid metabolism is my goal for the average psoriatic.
How about taking cla with squalene (sharks oil)?
Seems like a good fix to me!
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12196420&dopt=Abstract
Conjugated linoleic acid (CLA) is a group of dietary fatty acids with
antiobesity and antidiabetic effects in some animals. The trans10cis12
(t10c12) CLA isomer seems to cause these effects, including improved
insulin sensitivity. Whether such isomer-specific effects occur in
humans is unknown.
[snip]
These results reveal important isomer-specific metabolic actions of
CLA in abdominally obese humans. A CLA-induced insulin resistance has
previously been described only in lipodystrophic mice. Considering the
use of CLA-supplements among obese individuals, it is important to
clarify the clinical consequences of these results, but they also
provide physiological insights into the role of specific dietary fatty
acids as modulators of insulin resistance in humans.
So, cla will slow the production of leptin by fat cells. Which means
CLA
lowers TNF-alpha from those same cells and that means less
inflammation.
Thats a good thing for psor heads? YeP!
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12036077&dopt=Abstract
Concentrations of serum TNF-alpha and leptin were significantly
reduced by dietary CLA. (rat study)
I found about 20 hits on CLA and leptin. Most are animal (rat)
studies. The human trials seem to be ramping up only now.
But, how much are we like our lowly rat friends? We share the
genes for many identical pathways, but how often does mama rat
tell the teenage rats to go out and get some exercise?
Or, get a job Doby Gellis! You lazy rat!
Today's Dobies are on a different beat.
"Get off that rat rear end and move it away from that computer"
Heck, all MOM has to do it some feeding them and
they go out and forage on their own.
And what prompts them to run on that treadwheel?
Even in the rat world variations run ramPant.
http://ajpregu.physiology.org/cgi/content/abstract/285/1/R271
JXStern
>may not need it.
Hmm. Maybe I'll ask my housekeeper if she can score some for me.
Actually, I think they have it at TJ's now.
>Fixing lipid metabolism is my goal for the average psoriatic.
Hmm.
>So, cla will slow the production of leptin by fat cells. Which means
>CLA lowers TNF-alpha from those same cells and that means less
>inflammation.
>
>Thats a good thing for psor heads? YeP!
Hmm.
Dang, if we're so smart, why ain't we cured yet?
>Or, get a job Doby Gellis! You lazy rat!
That's Dobie Gillis to you. Zelda Gilroy is only my state senator,
and she's critical of having an actor as governator-elect, go figure.
Welcome to Kaliforneeya. Hey, Dobie worked in his Dad's store, it's
Maynard G. Krebbs who needed to get a job. "Work!?!??!"
J.