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1 23rd June 21:06
External User
Posts: 1
Default how long does Flaxseed oil stay good for?

if in the fridge and all, about how many weeks/months can it st used for?
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2 23rd June 21:06
External User
Posts: 1
Default how long does Flaxseed oil stay good for?

Saw something here


"It shouldn't smell funky,' Reinhardt-Martin said. 'Flax has a nutty flavor
and smell. It should smell good.' Reinhardt-Martin also warns that flaxseed
oil, which must be refrigerated, has a relatively short shelf life of a few
weeks. If the oil smells rancid, toss it. Flax seed oil should only be used
cold - it can't be heated like olive oil. Be sure to check the label closely
in the store and buy the organic variety where possible."

That seems like good advice.

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3 23rd June 21:08
External User
Posts: 1
Default how long does Flaxseed oil stay good for?

I've been buying and smelling it for a long time now (years) and
i haven't found any funky products. I would suppose they would
have to be negligent at the store and let it sit out for quite

Some flax products have a range of flavors due to the ingredients to keep it fresh.

I've heard that if its bad, you'll know. But i've taken any left
overs from my last four or so bottles and combined them into
one thats been in the fridge for eight months now and just
smelled it and nada. No smell at all. I certainly know its
way passed being fresh and only keep it to use on wood furniture outside.

Hi 123matt,

I suppose i go about six or seven weeks once its opened at the
Since i consume it every day (one tablspoon) its usually gone before
then. So stick with the 16oz. (473ml.) size unless your
getting benefit from two or more tablespoons a day. Which
seems excessive to me, but you won't know till you've
worked with it for awhile. You could try a half tablespoon three
times a day and depending on results cut back or increase.

If i'm understanding the theory,
the basic idea is to change the ratio of omega-6's to 3's
in your cell membranes. And those little dudes are constantly renewing
and dying. I read somewhere iirc that after seven years
all your cells have totally recycled. And if there's an
advantage to having a 4:1 ratio of n-6's to n-3's it should
show up over time. During flare season i find that if i stop
for a week or two i see and feel a marked difference.
Which may be accounted for by receptors on cells being kept
busy and not adding to the inflammation in general.
Its a cox-2 thing and recent articles from current research
has come up with a variant gene implicated in heart attacks.

The flax brand i'm using at the moment, Health from the Sun is
preserved with rosemary extract, vitamin C (ascorbyl palmitate)
and E (mixed tocopherols) and citric acid.

Rosemary oil is a phenol and some of us will have a problem with
it. So you may want to try other brands.

To flax or fish to get the omega-3's raises other questions.

And while flax seed oil has omega-3's some dispute whether its better
to try to get it from fish. Fish, known as brain food anecdotally
for years, has many abstracts as to its scientific

But what hope is there for attenuating psoriasis with
flax? It gets rather complex fast as these fats may act
as PPAR agonists, provided they are metabolized correctly (another
big if),

Should PPARs be used to upregulate a Th2 skew it would be
a neat trick as the benefits i find are slim and hard fought
for. And easily defeated with small amounts of arachidonic acid
foods and takes us back to other unclear areas of science.

Another good augmentation to the tablespoon of flax a day is
to increase the anti-ROS strategey,

Say you take the NAC and,14)+psoriasis&hl=en&lr=&ie=UTF-8&oe=UTF-8&

This isn't going where i want it to.
So time to segue over to topical ppar's in the news instead.

Someone wants to look at PPARg to stop diabetic inflammation
in this next hit.
Could PPARg be the ONE for syndrome X?,
Phipps' lab specializes in investigating the biomarkers for
inflammation. In experiments on human platelet samples, they
discovered that platelets express PPARg, a transcription factor that
was believed to be expressed only by cells with a nucleus. Activation
of the PPARg protein by certain anti-diabetic drugs blunts the ability
of platelets to release pro-inflammatory mediators and to form clots.
Studies are continuing on how PPARg alters platelet function, and the
group hopes to launch clinical research to test whether anti-diabetic
drugs dampen the inflammatory activity, and can be used to prevent or
treat vascular disease.

(What we've seen in the p group are other complications in using ppar
drugs. Blood pressure things and possible CoQ10 wasting etc.)


PPARs again? When is someone gonna figure them out?

Evetsm tried to find a ppar thing for syndrome X + P,
and link it to Psoriasis. And untill someone explains the fats
for P links, i'll keep wondering about it. And back to that delta
deoxy thing again and stereo fats (use hete's as a keyword for the

Back to diet,

From the previous link,
"Diet and exercise patterns are known to influence disease risk and
are a simple and effective way to tackle the spread of this disease.
In our modern society a combination of increased availability and
access to energy-dense convenience foods (that are high in fat, salt
and sugar) coupled with a limited need for physical activity, and
reduced opportunities for leisure-time active pursuits (due to hectic
working and social lives) all contribute to weight gain and a rise in

Practical steps to address these issues include the adoption of a
healthy balanced diet (as illustrated at, rich in fruit and vegetables
and with lower intakes of fat, sugar and salt, and an increase in the
levels of physical activity in our daily lives.

Whole article can be read at the British Nutrition Foundation:
================================================== ============================

And while evetsm ponders the paleo diet for less syndrome X, most
folks are
getting hooked uP with low carb (glycemic) atkins type diets now,

So what does all this have to do with P?

We don't know yet! We just know that some link to our P condition
may shine thru and help to explain our disease in the light of
unfolding current scientific research.
And with more of us reporting our findings to each other
and in particular while on biologicals, we build a database
of sorts as to what to expect. I get many great clues
here all the time. So don't stop bringing up those questions
and what if's.

Here's a new-ish fat clue with a hopeful link to our P fate,
They then identified the receptor as _prohibitin_, a protein which is
known to regulate cell survival and growth. "The expression of
prohibitin in organelles inside the cells such as the mitochondria,
and the nucleus, has been established, but its presence and function
on the cell surfaces of blood vessels associated with white fat tissue
has not been explored," says Arap. "We don't know what prohibitin is
doing there, but we know that this protein is not normally found in
blood vessels of several other tissues and also of tumors derived from
fat tissue."
Once that they had a "docking receptor" specific to white fat tissue,
the researchers designed a drug. They created a synthetic ligand - a
sequence of amino acids that would fit neatly into the prohibitin
receptor, like a key into a lock - and fused to it a corkscrew-shaped
"drug" that they knew could induce a cell to self-destruct.

P53 and prohibitin,
[snip] Prohibitin appears to induce p53-mediated transcription by
enhancing its recruitment to promoters, as detected by chromatin
immunoprecipitation assays. These results suggest that prohibitin is
capable of modulating Rb/E2F as well as p53 regulatory pathways.

PMID: 14500729

A possible key here to pregnancy immunity and P,

Another clue,

================================================== ================================================== ========================

If you read this far, i may as well stick the P news into
this post,
Small-molecule gene therapy nearing trials

- 10/05/2004 - A US company is gearing up to start trials of a novel
drug that could provide the first orally-active treatment for a range
of genetic disorders, including cystic fibrosis and muscular
dystrophy, writes Phil Taylor.

New Jersey-based PTC The****utics has asked the US Food and Drug
Administration for approval to start the trials of the lead candidate,
dubbed PTC124, in its Small Molecule Modulation of Read-Through
(SMMRT) programme.

Inherited diseases are attributable to mutations in an individual's
DNA. A common type of mutation, occurring in approximately 10 to 30
per cent of the cases of, leads to the synthesis of a messenger RNA
(mRNA) that contains an inappropriate stop codon – known as a nonsense
codon - within its protein-coding region.

This nonsense mutation causes the ribosome that reads the sequence and
assembles the protein to stop prematurely, producing a non-functional
protein. For example, in cystic fibrosis, the mutation prevents the
formation of a fully-functional protein called CFTR that is involved
in ion balance in the lungs and other organs.

PTC's drug is an orally-bioavailable small molecule that is designed
to prevent this inappropriate termination of protein production. The
programme stemmed from prior research showing that the antibiotic
gentamicin could restore the usual ‘read through' of the gene,
resulting in the expression of full-length CFTR protein.

Broad drug target in proliferative disorders

In other news, researchers at PTC have identified a new biochemical
pathway that could lead to a new generation of small-molecule drugs to
treat proliferative orders, including malignancies and psoriasis.

The company has discovered an enzyme complex that underlies the
metabolism of mRNA and a related molecule – transfer RNA (tRNA) – that
is integral to the process of cell proliferation.

Peltz said that the discovery, published in the journal Cell (30 April
issue) could lead to new treatments for haematological and solid
malignancies and inflammatory diseases such as psoriasis.

================================================== ============================

PTC124 stoPs nonsense mutations!

That sounds good,

And PTC's compounds modulate gene expression by selectively binding to
either RNA targets or to proteins that interact with RNA.
(Modulation is good!)

I don't know, after checking out this page on PTC.

They could have tossed the psoriasis WORD into the mix just to ***
things uP.

"Hey it may be good for P" they say with a wink and a nod.

That could bring in a few million more!

++++++++++++++++++++++++++++++++++++++++++++++++++ ++++++++++++++++++++++++++++++++++++++++++++++++++ +++

And as a sideline i checked out that godfather of enbrel and
TNF blockers, Ken Mohler's company.

Trubion's second family of pre-clinical candidates (TRU-016) target a
different B-cell receptor, and represent an alternative method for
depleting B-cells. TRU-017, in contrast, targets a non-B-cell receptor
for autoimmune applications. In addition, the Company is rapidly
expanding its pipeline through the development of SMIPs against an
array of other targets including important growth factor receptors,
co-stimulatory molecules, members of the tumor necrosis factor (TNF)
and TNF-receptor families, and targets on antigen-presenting cells.

SIMPs page,


^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ ^

And i may as well stick some inflammation things in also.

Can THC (from pot) fix the gut?

It would be fun trying!
Cannabinoids spell relief in colon inflammation

[snip] In the current issue of The Journal of Clinical Investigation
(15 April 2004) a researcher team from the Max Planck Institute of
Psychiatry and from the Ludwig-Maximilans-University Munich were able
to show that mutant mice lacking the cannabinoid receptor are much
more prone to experimentally induced colon inflammation as compared to
wild-type control mice.

Moreover, colon muscle activities become uncontrolled after
inflammation in these mutant mice. The treatment with cannabinoids was
able to alleviate inflammation in wild-type animals. Thus, these
results suggest that the endogenous cannabinoid system represents a
promising the****utic target for the treatment of chronic inflammatory
diseases of the gastrointestinal tract.

An important defense mechanism of the body after insults is the
induction of an inflammation. However, if this response is too strong
a destruction of the tissue may occur. Therefore, a balance between
pro- and anti-inflammatory responses is very important for the body.
Chronic inflammatory diseases of the gastrointestinal tract such as
Crohn's disease and Colitis ulcerosa constitute a widespread problem
in industrialized countries. These diseases are difficult to be
treated successfully and the search for novel the****utic approaches
is of high demand.

During centuries, extracts from Cannabis sativa have been used in folk
medicine for the treatment of various gastrointestinal diseases. The
most active compound of Cannabis sativa is
delta-9-tetrahydrocannabinol, also called THC.

The human body contains a receptor for THC and THC-like molecules, the
cannabinoid receptor type 1 (CB1). Body's fatty acid-like compounds,
called endocannabinoids, are also able to activate CB1 receptors. CB1
receptors and endocannabinoids are not only present in the brain but
also in the enteric nervous system. Recent investigations conducted by
researchers of the group of Beat Lutz at the Max Planck Institute in
Munich and of Martin Storr at the Medical Department II of the Ludwig
Maximilans University Munich suggest that the endogenous cannabinoid
system provides a protective mechanism to prevent excessive
inflammatory responses after an insult and thus helps to maintain the
balance between pro- and anti-inflammatory reactions.

Inflammatory responses were experimentally induced by infusion of a
sulfonic acid-containing substance into the colon of mice. In addition
to wild-type control mice, also CB1 knock-out mice (i.e. mice, lacking
the cannabinoid rececptor) were used. On day three after infusion, the
degree of inflammation was determined by different methods. CB1
knock-out mice showed a higher degree of inflammation as compared to
wild-type control mice.

Continue reading this article in the following web page:***entation/do***entation/pressReleases/2004/pressRelease20040506/

How come this next one sounds so familiar?

Transplant Rejection Averted By Simple Light Exposure In Stanford
Animal Study

STANFORD, Calif. - One of the unfortunate side effects of bone marrow
and stem cell transplantation is that the newly implanted cells often
stage an internal attack against the patient they're intended to help.
Stanford University School of Medicine researchers now have a better
grasp of this phenomenon, known as graft-versus-host disease, or GVHD,
and have proposed a possible method of prevention: simple ultraviolet

In a new animal study, researchers identified the principal culprit in
GVHD: an immune cell in the skin known as a Langerhans cell. These
cells normally function as flag posts for the immune system, signaling
infection-fighting T-cells to come to a particular site to fight off a
virus or bacteria. But in transplants, they do patients a great
disservice, alerting T-cells to attack the patient's own tissues,
researchers found.

The researchers were able to effectively eliminate the Langerhans
cells in transplanted mice by exposing them to ultraviolet light,
giving the animals mild sunburn. Transplanted mice that received this
treatment experienced no GVHD while those that didn't showed severe
signs of the disease, said Edgar Engleman, MD, professor of pathology
and medicine and senior author of the study.

"The experiment not only provided the proof that these cells cause
graft-versus-host disease, but also provides a way of thinking about
how you might prevent it," said Engleman, who also directs the
Stanford Blood Center. The study appears in the May issue of the
journal Nature Medicine.

Bone marrow or stem cell transplants are commonly used to treat
patients with cancers of the blood system, such as leukemia, lymphoma
or myeloma. Patients first receive radiation treatment to wipe out
their defective immune systems, which then are replaced by healthy
donor cells.

Sometimes, however, the process fails as GVHD sets in. The effects of
the disease are most commonly seen in the skin as a reddish rash or,
in more severe cases, as skin that blisters and peels.

The Stanford scientists first suspected that Langerhans cells might
have a major role in GVHD after their earlier experiments showed these
cells were resistant to radiation and persisted in the skin for a long
time, said Miriam Merad, MD, PhD, a former postdoctoral scholar in
Engelman's lab and the first author of the study. The discovery was
"shocking," Engleman said, as all other white blood cells have a short
half-life and are frequently replaced. The Langerhans cells don't
change unless they're disturbed in some way, say by inflammation, he

(Ah ha!-- clue isn't it?)

The scientists surmised that these cells might linger in the skin of a
transplant patient and instigate trouble. Their latest experiments
bore this out.

The researchers tested their theory in two different sets of mice. In
one group, the animals had their own Langerhans cells intact. When
these animals were transplanted, the Langerhans cells triggered a
response and the mice developed severe GVHD. In a second group, the
scientists replaced the animals' Langerhans cells with other cells.
When these mice underwent transplant, they remained protected from

The scientists took it a step further. They exposed the vulnerable
mice - those with their own Langerhans cells - to ultraviolet light
using a sunlamp. The sun exposure depleted the Langerhans cells and
effectively protected the mice from the disease, said Merad, who is
now based at the Mount Sinai School of Medicine.

The researchers said the results present a promising option for
transplant patients and could be the basis for clinical trials in
which patients are exposed to ultraviolet light before treatment.

"What we would do is try to eliminate the host Langerhans cells before
the transplant, as we did in the mice," Merad said. She noted that
dermatologists now use ultraviolet light to treat some skin diseases,
administering it to patients inside a chamber under controlled
cir***stances to avoid burning.

Engleman said the ultraviolet treatment would have to be carefully
administered to patients before bone marrow or stem cell
transplantation to avoid harmful side effects. "The trick is deplete
the host Langerhans cells in a manner that doesn't cause other
unwanted effects," he said.

(Does this explain the seasonality of P?)

================================================== ================================================== ============================

Heart attack gene?


The heart attack patients were significantly more likely to carry a
specific mutation in a gene that produces a protein called galectin-2.

Galectin-2 is known to bind to a molecule that assists inflammation -
lymphtoxin-alpha (LTA) - and which is released when a coronary artery

The gene mutation appears to change galectin-2, and in turn to affect
the amount of LTA that is secreted - possibly boosting inflammation
and increasing the risk of a heart attack. [snip]
Gene Variant May Cut Risk of Heart Attack
Researchers have identified a genetic variation in some people that
appears to reduce their chances of a heart attack or stroke - even in
those with high blood pressure, high cholesterol or other risky
conditions. [snip]
Cipollone and colleagues found that a guanine to cytosine substitution
at position –765 of the cyclooxygenase 2 gene is associated with a
lower risk of myocardial infarction (MI) and ischemic stroke.

Heart attack could be in a gene
People with a variation in a gene that encodes for a protein called
galectin-2 may face a much higher risk of myocardial infarction, their
study, published yesterday in the British weekly journal Nature,
said.One of the significant players in this event is the molecule
cytokine lymphotoxin-alpha (LTA), which helps to regulate
inflammation, a result of the emergency call upon the body's immune
system.Scientists led by Toshihiro Tanaka at the Institute of Physical
and Chemical Research in Tokyo found that levels of LTA are determined
by the lectin protein galectin-2.And, in turn, levels of galectin-2
depended on variations in a gene, LGALS2, which controlled this
protein.In lab-dish tests, they found that one of three variations
they studied could reduce galectin-2 by half - a huge fall that they
hypothesise is bound to have an effect on secretions of LTA.

the end.
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