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IRON - Immunities --->Inflammation & Fe--> Discombobulation -->HEPCIDIN (Levels) -- Touch ( Reflexology) - OccyPy Golf Movement -- MUC1 (Mucin / Mucus) Cancer Vaccine -->Sarkis Mazmanian & Khosravi H. Pylori
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randall
Apr 9, 2012, 6:11:24 PM4/9/12
to
hi
Are you FAT becaUSE YOU eat twinkies all day LONG?
Should obamacare allow obese people to get pregnant if your chance of
having an autistic child is
in 55 or higher due to low glutathione (NAC) levels?
Should you be allowed to take tyelenol (Acetaminophen), which lower's
GLUTATHIONE (NAC), if pregnant?
And what about being and eating IRON?
Certainly women have a monthly release valve on iron....
Should obamacare order men to have a period to give blood
and thereby lower IRON levels? To EVEN things OUT?
Should women have to take testosterone after menopause then?
What will obamaCARE care about? You, me or the goons of gov run by
goonunions:
http://www.hillsdale.edu/images/userImages/mvanderwei/Page_6907/Imprimis_March12.pdf
What Public Employee Unions are Doing to Our Country
William McGurn
<snip>
Is goonulism due to excess iron (red meat) in their diets? How do we
put the gov on a DIET?
OTOH (on the other HAM.... easter you know... LOL)
What if your iron is already to LOW due to being a VEGAN perhaPs?
But, but, but.... LANCE ARMSTRONG is vegan : NOW:
http://www.ecorazzi.com/2012/04/09/lance-armstrong-fuels-fitness-with-a-mostly-vegan-diet/
How does he suPPlement to keep his minerals optimum?
------------------------------------
IRON MAN & Women ALERT...... not Robert Downey or Gwyneth Paltrow...
of course...
Iron IS in the FIREs of LIfE?
Who KNEW low iron is caused by excess INFLAMMATION?
REALLY... no...REALLY?
WHO SAID so?
Byron KNOWs in the next article:
Psor people are full of inflammation and the more severe the wORSE it
is...
Hey! Don't BE severe!
:(
Yikes... i've got it.... how do i stoPPer it?
er er er...?
And with NO to LOW--> ENERGY in me MITO's..... yikes..
STAT to the ER and fity grams of Fe for me?
From: BYRON Today:
http://www.wellnessresources.com/weight/articles/stunning_discoveries_regarding_iron_obesity_candida_thyroid/
Stunning Discoveries Regarding Iron, Obesity, Candida & Thyroid
Friday, April 06, 2012 - Byron Richards
The information contained in this groundbreaking article applies to at
least 75 percent of people who are struggling to lose weight. It is a
major factor contributing to the fatigue associated with being
overweight and having symptoms of hypothyroid. It involves new
discoveries regarding iron metabolism and explains why even if you eat
plenty of iron you may still have rather dramatic iron deficiency
issues, which handicap your metabolism and thyroid function.
Traditional thinking about iron is that either you get enough in your
diet or you don’t. People who don’t eat red meat, menstruating women,
those who exercise a lot, and those with digestive bleeding or other
blood loss issues are at risk for iron deficiency, and either
functional or blatant anemia. In general, iron deficiency is thought
to be associated with undernutrition or malnourished states.
Ironically, in the past few years, it has become clear that at least
half the people who are overweight have impaired iron metabolism
detectable on blood tests. In many of these cases dietary iron intake
was adequate, perplexing researchers. It now appears that the
inflammation associated with being overweight is elevating a hormone
in your liver called hepcidin, which has the net effect of reducing
iron absorption into your body from your digestive tract. The net
result is a metabolic nightmare of weight gain, fatigue, and poor
thyroid function.
Hepcidin 101
Hepcidin is a hormone produced in your liver, discovered in the year
2000. Scientists have discovered that it regulates iron use
throughout your body (iron homeostasis). One of the ways hepcidin
regulates your iron status is by deciding how much iron to let in to
your body. In essence it communicates directly to the cells of your
digestive tract, either allowing them or not allowing them to let iron
in. High levels of hepcidin reduce or prevent dietary iron intake
into your body, regardless of the iron content of your food.
It is now clear that hepcidin levels elevate in response to
inflammation. This could be from inflammation of any type: infection,
toxin exposure, excess alcohol, many medications, injury, excess
exercise, lack of sleep, too much stress, etc. In this regard, being
overweight is an ongoing inflammatory problem wherein your extra
pounds of white adipose tissue crank out inflammatory signals 24 hours
a day, 7 days a week, as if someone will not stop yelling at you. The
more excess weight you have, the higher the inflammation (in addition
to all other potential sources of inflammation).
Iron is utterly indispensable to your metabolism and survival. For
example, mice that are genetically bred to have high levels of
hepcidin die within a few days from iron deficiency. Iron is need for
growth, repair, assembly of proteins into your body structures, the
function of your nerves, and much more.
On the other hand, iron is highly reactive. Your body literally keeps
it in cages like ferritin, kind of like a lion at the zoo. When it is
needed, the lion is let out at the proper place and time so that it
can do something useful. If the cage is opened at the wrong time or
place then iron can jump out and set off free radical chain reactions
that can be very damaging to health. It appears that hepcidin
intentionally reduces iron intake during times of inflammatory stress
to prevent the inflammation from damaging iron transport and storage
systems (causing inappropriate iron release). In other words, if your
body is in a state of inflammatory wear and tear it may be difficult
to use iron in a healthy way.
This would offer excellent survival features for short term
inflammatory distress that are threats to survival. However, a
chronically inflamed person, as from obesity, can develop a real
catch-22 wherein hepcidin is elevated for too long, which creates a
scenario of ongoing iron deficiency, either functional (meaning not
enough iron for metabolism to function well) or blatant (meaning
anemia).
Due to the rampant overuse of antibiotics and high sugar diets of many
people there is an epidemic of Candida albicans overgrowth in
overweight people. This is especially common in overweight people
with thyroid problems, as I have observed first hand for the past 27
years. Interestingly, hepcidin is a powerful antifungal. This means
that your body may raise its hepcidin levels to prevent Candida from
infiltrating your body, which is part of a natural defense system.
Again, this has survival advantages especially in olden times.
However, in a population of people who are overweight and have an
overgrowth of antibiotic-induced Candida, it is a double whammy
against a functioning metabolism.
The Impact of Low Iron on Metabolism
A new study details the dire metabolic consequences of having low
iron. It shows that low iron turns on genes in your liver and muscles
that promote fat storage and cause abnormal elevation of blood sugar –
exactly what goes wrong with metabolism that leads to the metabolic
syndrome.
The consequence to thyroid metabolism is twofold. First, the inactive
thyroid hormone,T4, is converted to the biologically active
hormone,T3, mostly on cell membranes of liver cells. Hepcidin is made
in your liver and is being produced excessively in response to high
inflammation. Such inflammation will also damage liver cell
membranes, thus reducing the conversion of T4 to T3. This is one main
reason why inflammation of any type disturbs thyroid function.
Second, when biologically active thyroid, T3, binds on to cell
membranes and communicates to the nucleus of your cells how fast their
metabolic pace should be set, it is like a hormone manager giving an
order to a cell factory. The worker bees in the cell factory then
need iron for the genes that will implement the thyroid order. In
fact, the next 80 metabolic genes responding to a thyroid order all
need iron. If iron is lacking metabolism simply cannot run at an
optimal pace, which will give a person all the symptoms of hypothyroid
even if they have normal T4 and normal T3.
Iron can be normal on a blood test and a person can still have all the
problems above, though levels tend to be toward the lower end of the
normal range. Hemoglobin (Hgb) and hematocrit (Hct) are also on the
low side of the normal range with this problem. If one or another is
out of range on the low side it signifies a major problem. Serum
ferritin is typically low or low normal, unless inflammation is very
high, which can actually drive up ferritin scores. Lab tests can
help, however, fatigue along with trouble losing weight despite eating
better and exercising are general indicators of a potential problem.
Solving Iron Deficiency relating to Stubborn Weight
Adequate iron intake (red meat) compared to obvious iron loss
(menstrual cycles, etc.) is still important to understand. However,
this new data says that a condition of less inflammation must exist in
order for iron to work properly in your body.
The most basic approach is to follow The Leptin Diet, which is anti-
inflammatory. As you begin to lose weight you are now reducing
inflammation, hepcidin levels should come down, and the iron in your
diet will work better. If you have little iron in your diet, then you
should take a high quality iron supplement. I like iron glycinate, a
true protein chelate of iron. I would stay away from all cheap iron
salts, such as ferrous sulfate (these cause free radical damage).
In reality there are many basic supplements that are fundamental to
metabolism along with a good diet, as I have outlined in The Leptin
Diet Weight Loss Challenge #1 – Overview and Basic Needs. All of
these are important to contribute to anti-inflammatory basic
nutrition. Based on the new information in this article, it is
accurate to say that ensuring you have adequate iron intake should be
added to this basic list of nutrient needs for weight loss, especially
in conjunction with basic anti-inflammatory nutrition.
A more comprehensive approach to this specific issue is to take an
iron supplement as a trial to see if it helps your energy.
Additionally, fat-soluble antioxidants that are targeted to improve
liver function would be top choices. My top recommendations would be
acetyl-l-carnitine, coenzyme Q10, tocotrienol E, r-alpha lipoic acid,
and silymarin. Many other anti-inflammatory nutrients may also be of
value. Your bottom line is to get enough support to engage the
process of weight loss, maintain steady progress, have a much better
energy level, and on a blood test your hemoglobin and hematocrit
should be in the middle of the normal range.
Some individuals may need to employ a more targeted anti-Candida
program to fully solve this problem. I discuss these topics more
fully in my series of comprehensive articles on the Leptin Diet Weight
Loss Challenge. It is important to know the direction you are
heading. If you are doing well and making progress then you are most
likely doing enough – at least as long as you are getting somewhere.
If you hit a plateau or fail to get out of the starting block then you
certainly need to become an active problem solver for your metabolic
issues. Hepcidin issues are far more common than not in any person
who struggles with weight.
Summary
Your body handles iron as a top priority, since it is vital to
survival as well as being potentially problematic. Iron is essential
for metabolism to run properly, including normal thyroid activation
and cellular function. The inflammation of obesity is elevating a
hormone called hepcidin, which has the unfortunate side effect of
disrupting iron metabolism in your body. This mechanism helps you
overcome short term inflammation and was very handy in olden times for
survival purposes. In modern times, especially in a population of
overweight people who often have Candida issues, it can viciously lock
in place malfunctioning metabolism. Solving the problem requires
adequate iron intake along with a reduction in inflammation. Reducing
life stress helps. Sleeping better helps. Following The Leptin Diet
helps. Many dietary supplements can also help reduce inflammation.
Especially important may be the fat-soluble antioxidants that help
reduce liver inflammation, the place of hepcidin synthesis. Use
enough support to feel a difference in your energy level while
engaging and sustaining the process of healthy weight loss. There is
a path to a healthier you!
<snip>
------------
24 hits for mito DNA - p ng
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=mitochondrial+dna&start=0&
Is one of 24 the clue for fatigue?
Why Autoimmune people are so depressed is ER?
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/c2686d542d831738/31051264331a0bc7?lnk=gst&q=mitochondrial+dna#31051264331a0bc7
So give some credit to : Ward Dean, M.D., and Steven Wm. Fowkes
http://www.ceri.com/mito.htm
<from: psors1rnaDNAsilencing>
--------------
^^^^^^^^^^^^^^^^^^^^^^^^
Touch ME now...
The Doors - Touch Me
http://www.youtube.com/watch?v=4UEVyIyibD8
http://www.vrp.com/stress/take-on-anxiety-with-the-power-of-touch?utm_content=article3511
TAKE ON ANXIETY WITH THE POWER OF TOUCH
A grueling commute, a high-pressure job, a shrinking 401K or mounting
family demands… when you’re burning the candle at both ends, it may
seem like the only way to escape the chaos is a one-way ticket to the
nearest private island. But what if you could get a break from the
daily onslaught of stress without packing a single bag?
As it turns out, a permanent vacation isn’t the only way to give your
mind and body some much needed respite. A growing body of research
shows that an alternative therapy called reflexology may also be an
effective antidote to health-robbing anxiety.
The Healing “Zone”
So what is reflexology, exactly?
Well, similar to practices like acupressure and acupuncture,
reflexology relies upon a complex map of designated points on the
hands, feet and ears—so-called “zones” or “reflex points”—that
correspond to various organs and systems in your body.
According to the principles of reflexology, applying purposeful
pressure to these specific points can help to balance the body’s
energy and affect the function of corresponding systems, yielding
powerful therapeutic effects—such as pain relief, increased energy
and, of course, anxiety reduction.
As a healing method, reflexology has enjoyed a long history, appearing
in records as far back as ancient Egypt. Its first introduction in the
United States dates back to the early 20th century—but even modern
science supports its use in dealing with everyday maladies, with
published studies pointing to the effectiveness of reflexology when
used by itself or as part of a larger complementary health strategy.
Mind-Body Stress Relief… and More
In a pilot study published in January 2004, 30 healthy subjects
received either reflexology or no treatment, with the latter group
serving as a control. Researchers assessed each participant for self-
reported anxiety, stress-related heart parameters (including blood
pressure and heart rate) and salivary levels of cortisol and melatonin—
two hormones directly involved in the body’s stress response—both
before and after the reflexology treatments.
Results showed that reflexology had powerful anti-anxiety benefits,
reducing both anxious states in the subjects, as well as blood
pressure and heart rates.1 In fact, the outcome was promising enough
that the researchers intend to transfer their findings to a new study
involving women with breast cancer—a circumstance under which
reflexology’s stress-modulating effects may be particularly
pronounced, due to the prevalence of cortisol and melatonin imbalances
in these patients.
In the meantime, the potential benefit of this calming natural cure is
clear. Considering the dangerous link between chronic stress and a
long list of serious health problems—from reduced immunity and
increased inflammation to higher risk of heart disease and cancer—it’s
easy to see how reflexology could end up playing a vital role in
therapeutic protocols for any number of conditions.
It’s also no surprise that published research already backs up
reflexology as a drug-free form of relief for anything from menstrual
pain, backache and constipation to fibromyalgia and even Parkinson’s
disease.2-6
To find a qualified reflexology therapist in your area, you can
perform a simple search through the Reflexology Association of
America. Your frazzled nerves will thank you for it.
References:
<snip>
^^^^^^^^^^^^^^^^^^^
Isn't this next one predicated on levels of iron and iodine etc?
Or selling some genetic analysis?
23andMe identifies 5 significant genetic associations for
hypothyroidism
April 9, 2012 in Genetics
Using its unique online research platform, 23andMe, a leading personal
genetics company, has found five significant genetic associations for
hypothyroidism in the largest known genome-wide association study of
hypothyroidism conducted to date. The details of the study are now
available online in the journal PLoS ONE.
"With nearly 90 percent of our 125,000 customers participating in our
online research, 23andMe is making crowd-sourced science a reality,"
stated 23andMe CEO and co-founder Anne Wojcicki. "Our online research
platform continues to advance research faster and more cost
effectively than traditional research models," added Wojcicki.
Of the five significant associations reported in this study, three are
known to be involved in other autoimmune diseases. These include
rs6679677 near PTPN22, rs3184504 in SH2B3, and rs2517532 in the HLA
class I region. The other two associations reported here are rs4915077
near VAV3 and rs925489 near FOXE1, a gene involved in thyroid
development. In addition, 23andMe observed associations with two loci
marginally associated with hypothyroidism that have been linked to
Thyroid Stimulating Hormone (TSH) levels, PDE8B and CAPZB as well as
another gene previously associated with hypothyroidism and autoimmune
disease (CTLA4).
"These genetic associations contribute significantly to understanding
the underlying biology of hypothyroidism, which impacts five percent
of the general population," remarked 23andMe Medical Director and
study co-author Dr. Uta Francke. "Identification of associations with
other autoimmune disorders opens up potential pathways of treatment."
Upon identification of those novel genetic associations for
hypothyroidism also associated with autoimmune diseases, the 23andMe
research team looked for any additional single-nucleotide
polymorphisms (SNPs) shared with other autoimmune diseases,
investigating a list of 107 SNPs that were studied across seven
autoimmune diseases. Among this list, only the CTLA4, PTPN22, and
SH2B3 loci show significant association with hypothyroidism.
According to 23andMe Principle Scientist and Lead Author Nicholas
Eriksson, Ph.D., "These findings shed new light on the biology of
hypothyroidism, showing that genes involved with both thyroid function
and immune response impact this disease. This demonstrates our ability
to harness the power of the enormous 23andMe genetic database to
further medical research.
This study investigated 3,736 individuals with hypothyroidism as well
as 35,546 controls, all drawn from the more than 100,000 23andMe
customers who have consented to participate in research efforts. Cases
included individuals who have been diagnosed with hypothyroidism, have
elevated TSH levels, or are taking thyroid hormone replacement
medication.
These results continue to validate 23andMe's methodology in combining
self-reported data on phenotypes gathered via web-based questionnaires
and genotypic data derived from self-collected saliva samples. 23andMe
had previously published its first proof-of-concept results in the
journal PLoS Genetics in June 2010 which reported novel associations
for unusual traits such as asparagus anosmia and photic sneeze reflex
and replicated associations for other common genetic traits, and
recently published the discovery of two novel genetic associations for
Parkinson's disease in PLoS Genetics, and presented a major
replication study of over 180 genetic associations in the journal PLoS
ONE in August 2011.
<snip>
^^^^^^^^^^^^^^^^^^
THE
"OCCUPY GOLF" MOVEMENT
WE NEED TO BE HEARD!!!
I am a member of golf ’ s lower 99%.
I am an indifferent golfer,
there i s no way I could ever make it
to the professional level.
I will never put in the practice
Time to be the best.
I will never have the shots,
skills, or mental toughness
to make it in the sport.
I just never felt like working
all that hard at it.
However,
I am a part of the
golfing community,
as such,
feel I should be paid
by the top 1% of golfers
for what I do.
It isn't fair that those players
who have worked harder,
have studied the game
more carefully,
have better equipment,
are more skilled and dedicated
should make all that BIG money.
Where's my share?
I a m a Victim!
The top 1% should pay for
my club memberships
and green fees and lessons,
buy me new clubs, balls,
clothes and shoes, and
pay me some of their winnings.
They can afford it.
They are The Rich .
The whole system should be changed
to accommodate people like me.
I think we should get together
and "occupy" a golf course;
demand that those who are
better at what they do,
pay for us who generally suck.
Whining should get us something -
maybe we'll make the cover of
Time Magazine
And garnish some public sympathy.
Hell, during this election year,
we may even get a law or two
passed by legislators who want
our votes.
The "Occupy Golf "Movement
P.S. – Don ’ t mention this to tennis players!
We thought of it first!!!
We are planning to occupy the front
of the gate at the Masters this year.
remember i t’s for the 99%.
Bring your signs
^^^^^^^^^^^^^^^^^^^^^^^
And if you can't relax and have zero energy and risk getting cancer
as your gut microbiota are funky.... then fix the muck gene.
Muc1 <<mucins and mucus in your Gi TRACT-- think pancan and black
cohosh?>>
see
http://en.wikipedia.org/wiki/MUC1
http://www.dailymail.co.uk/health/article-2127238/Universal-vaccine-tackle-90-cent-cancers-tested-humans-time.html
'Universal' vaccine that could beat 90 per cent of cancers is tested
on humans for first time
Vaccine triggered greater immunity to cancer cells in trial patients
By FIONA MACRAE and CLAIRE BATES
UPDATED: 08:44 EST, 9 April 2012
A vaccine that targets a molecule in 90 per cent of all cancers has
been tested on humans for the first time.
Results from the safety trial - on patients with blood cancer - found
all had greater immunity to the disease after receiving the vaccine.
Three of the seven patients who have completed the treatment are now
free of the condition.
As a therapeutic vaccine it is designed to be given to patients to
help their bodies fight cancer rather than the majority - known as
prophylactic vaccines - that aim to prevent disease in the first
place.
Researchers believe the jab could also tackle breast, prostate,
pancreatic, bowel and ovarian cancers
Even tumours that resist treatment with the best medicines on the
market, including the breast cancer ‘wonder drug’ Herceptin, may be
susceptible to the vaccine.
If all goes well, the vaccine – called ImMucin – could be on the
market by 2020.More than 300,000 cases of cancer are diagnosed in
Britain each year and the disease kills around half this number
annually.
Rather than attacking cancer cells, like many drugs, the new treatment
harnesses the power of the immune system to fight tumours.
The search for cancer vaccines has until now been hampered by fears
that healthy tissue would be destroyed with tumours.
Researchers from the drug company Vaxil Biotheraputics and Tel Aviv
University have focused on a protein called MUC1 that is made in
bigger amounts in cancerous cells than in healthy ones.
Not only is there more of it, but a sugar that it is ‘decorated’ with
has a distinctive shape.
The vaccine ‘trains’ the immune system to recognise the rogue sugar
and turn its arsenal against the cancer.
The misshaped MUC1 sugar is found in 90 per cent of all cancers. There
have been ‘dramatic’ results in tests on mice with breast tumours.
Now, Vaxil Biotheraputics have announced promising results in a human
safety trial.
Ten patients suffering from multiple myeloma, a form of blood cancer,
have now received the vaccine received the vaccine at the Hadassah
Medical Centre in Jerusalem.
Seven of the patients have finished the treatment and Vaxil reported
that all of them had greater immunity against cancer cells compared to
before they were given the vaccine. Of the seven, three patients are
reportedly free of detectable cancer.
None of them have reported suffering side-effects apart from minor
irritation.
A statement from Vaxil Biotheraputics said: 'ImMucin generated a
robust and specific immune response in all patients which was observed
after only 2-4 doses of the vaccine out of a maximum of 12 doses.
'In some of the patients, preliminary signs of clinical efficacy were
observed.'
Years of large-scale human trials will be needed before the drug is
judged safe and effective for widespread use in hospitals.
It could then be used with existing drugs to boost treatment and given
to prevent tumours from coming back after surgery.
Men and women known to be at high risk of cancer because of their
genes could also be vaccinated in an attempt to stop tumours from
appearing.
Dr Caitlin Palframan, of Breakthrough Breast Cancer, said: ‘This
exciting new approach could lead to treatments for breast cancer
patients who have few options.
‘It also opens up the possibility of vaccinating high-risk women
against breast cancer in the future.'
<snip>
http://en.wikipedia.org/wiki/MUC1
Mucin 1, cell surface associated (MUC1) or polymorphic epithelial
mucin (PEM) is a mucin encoded by the MUC1 gene in humans.[1] MUC1 is
a glycoprotein with extensive O-linked glycosylation of its
extracellular domain. Mucins line the apical surface of epithelial
cells in the lungs, stomach, intestines, eyes and several other organs.
[2] Mucins protect the body from infection by pathogen binding to
oligosaccharides in the extracellular domain, preventing the pathogen
from reaching the cell surface.[3] Overexpression of MUC1 is often
associated with colon, breast, ovarian, lung and pancreatic cancers
[...] Role in Cancer
The ability of chemotherapeutic drugs to access the cancer cells is
inhibited by the heavy glycosylation in the extracellular domain of
MUC1. The glycosylation creates a highly hydrophilic region which
prevents hydrophobic chemotherapeutic drugs from passing through. This
prevents the drugs from reaching their targets which usually reside
within the cell. Similarly, the glycosylation has been shown to bind
to growth factors. This allows cancer cells which produce a large
amount of MUC1 to concentrate growth factors near their receptors,
increasing receptor activity and the growth of cancer cells. MUC1 also
prevents the interaction of immune cells with receptors on the cancer
cell surface through steric hindrance. This inhibits an anti-tumor
immune response.[2]
Preventing Cell Death
MUC1 cytoplasmic tail has been shown to bind to p53. This interaction
is increased by genotoxic stress. MUC1 and p53 were found to be
associated with the p53 response element of the p21 gene promoter.
This results in activation of p21 which results in cell cycle arrest.
Association of MUC1 with p53 in cancer results in inhibition of p53-
mediated apoptosis and promotion of p53-mediated cell cycle arrest.
[17]
Overexpression of MUC1 in fibroblasts increased the phosphorylation of
Akt. Phosphorylation of Akt results in phosphorylation of Bcl-2-
associated death promoter. This results in dissociation of Bcl-2-
associated death promoter with Bcl-2 and Bcl-xL. Activation was shown
to be dependent on the upstream activation of PI3K. Additionally, MUC1
was shown to increase expression of Bcl-xL. Overexpression of of MUC1
in cancer. The presence of free Bcl-2 and Bcl-xL prevents the release
of cytochrome c from mitochondria, thereby preventing apoptosis.[18]
MUC1 cytoplasmic tail is shuttled to the mitochondria through
interaction with hsp90. This interaction is induced through
phosphorylation of the MUC1 cytoplasmic tail by Src (gene). Src is
activated by the EGF receptor family ligand Neuregulin. The
cytoplasmic tail is then inserted into the mitochondrial outer
membrane. Localization of MUC1 to the mitochondria prevents the
activation of apoptotic mechanisms.[19]
Promoting Tumor Invasion
MUC1 cytoplasmic tail was shown to interact with Beta-catenin. A
SXXXXXSSL motif was identified in MUC1 that is conserved with other
beta-catenin binding partners. This interaction was shown to be
dependent on cell adhesion.[20] Studies have demonstrated that MUC1 is
phosphorylated on a YEKV motif. Phosphorylation of this site has been
demonstrated by LYN through mediation of interleukin 7,[21] Src
through mediation of EGFR,[22][23] and PRKCD.[24] This interaction is
antagonized by degradation of beta-catenin by GSK3B. MUC1 blocks the
phosphorylation-dependent degradation of beta-catenin by GSK3B.[25]
[26] The end result is that increased expression of MUC1 in cancer
increases stabilized beta-catenin. This promotes the expression of
vimentin and CDH2. These proteins are associated with a mesenchymal
phenotype, characterized by increased motility and invasiveness. In
cancer cells, increased expression of MUC1 promotes cancer cell
invasion through beta-catenin, resulting in the initiation of
epithelial-mesenchymal transition which promotes the formation of
metastases
<snip>
8 hits: iron muc1 -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=muc1%20iron
1941 hits : muc1 cancer
http://www.ncbi.nlm.nih.gov/pubmed?term=muc1%20cancer
20 hits: mucin FRAGILIS - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=mucin%20fragilis
<note: zero hit: fragilis muc1 etc>
And #2 of 20 being so KEY.....to me anyWHEY...
http://www.ncbi.nlm.nih.gov/pubmed/21664470
The human commensal Bacteroides fragilis binds intestinal mucin.
Huang JY, Lee SM, Mazmanian SK.
Anaerobe. 2011 Aug;17(4):137-41. Epub 2011 Jun 2.
PMID: 21664470
And since Sarkis is my FAVORITE due to fragilis binding...s
Then we look at his most recent...
And no MEAT in the taco.... Bummer ...
http://www.ncbi.nlm.nih.gov/pubmed/22481405
Nat Med. 2012 Apr 5;18(4):492-4. doi: 10.1038/nm.2723.
Breathe easy: microbes protect from allergies.
Khosravi A, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena,
California, USA.
PMID: 22481405
Since i know what SK is doing...we look at
80 hits: "Khosravi A"[Author] -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosravi%20A%22%5BAuthor%5D
The ONE that caught my attention
#8 of 80
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22291830/?tool=pubmed
http://www.ncbi.nlm.nih.gov/pubmed/22291830
Arch Med Sci. 2011 Oct;7(5):844-9. Epub 2011 Nov 8.
Evaluation of Helicobacter pylori infection in patients with common
migraine headache.
Hosseinzadeh M, Khosravi A, Saki K, Ranjbar R.
Source
Department of Immunology, Faculty of Medicine, Ilam University of
Medical Sciences, Ilam, Iran.
Abstract
INTRODUCTION:
Migraine can cause headache in different communities so that 12-15%
are suffering worldwide. Recently the relationship between infectious
diseases such as Helicobacter pylori infection and migraine headache
has been the focus of many studies. The current study was designed to
evaluate IgG and IgM antibodies to H. pylori in patients suffering
from migraine headaches.
MATERIAL AND METHODS:
Patients who had diagnostic criteria for migraine were chosen as cases
compared to some healthy individuals as the control group amongst
which immunoglobulin G (IgG), immunoglobulin M (IgM), age, job, gastro-
intestinal (GI) disorders, history of migraine, special meals,
medications, sleeping disorders, stress, environmental factors etc
were analysed.
RESULTS:
The prevalence of disease was 38.6%. Household women had the highest
prevalence (40%). Among them menstruation was related to high
prevalence of migraine. 75.6% of patients had gastrointestinal
disorders of which the gastric reflux was the most important sign
(47.1%). The mean optical density (OD) value of IgG and IgM antibody
to H. pylori was 60.08 ±7.7 and 32.1 ±8.7 for the case group, 21.82
±6.2 and 17.6 ±9.4 for the control group, respectively.
CONCLUSIONS:
There was a significant difference in mean OD value of both antibodies
to H. pylori amongst the case and control groups. As a result, active
H. pylori infection is strongly related to the outbreak and severity
of migraine headaches, and H. pylori treatment reduces migraine
headaches significantly. Hopefully, the definite treatment and
eradication of this infection can cure or reduce the severity and
course of migraine headaches significantly if not totally.
PMID: 22291830
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22291830/?tool=pubmed
#20 of 80 helps give a GUT perspective on IRON and what hepcidin Byron
in the first article
tells US.
http://www.ncbi.nlm.nih.gov/pubmed/21526105
J Res Med Sci. 2010 Nov;15(6):324-30.
The antibody titers to Helicobacter pylori in 7 - 12 year old iron
deficiency anemic children, in Ilam.
Hoseinzadeh M, Khosravi A, Sayemiri K, Rasoli MH, Mohaveri A.
Source
Immunology, Ilam University of Medical Sciences, Ilam, Iran.
Abstract
BACKGROUND:
It has recently been revealed that H. pylori infection is one the most
important causes of anemia inhibiting iron uptake. The current study
was designed to evaluate the correlation between the iron deficiency
anemia and IgG to H. pylori in anemic children.
METHODS:
In this analytical study, 100 anemic children were analyzed using
total Iron, Ferritin, TIBC and H. pylori IgG assay. Data were
collected using a questionnaire including parameters of age, blood
group, infancy nutrition, iron consumption, fatigue, weakness, height,
weight, gastrointestinal infectious, parasitic and blood diseases,
parent literacy, income, inhabitation, etc. Data were analyzed using
Multivariate Regression Analysis Models, Pearson Correlation- test and
Kolmogrov Smirnov.
RESULTS:
The most prevalent blood group detected in the study sample was group
O (62%); 79% were breastfed, 9% were bottle- fed, 12% were both
breastfed and bottle- fed. The history of gastrointestinal disorders
was mentioned amongst 91% of the patients' family members. A
significant relationship was observed between the iron level with
serum, ferritin, level of TIBC and elevated level of IgG titer to H.
pylori (p < 0.001). There was a significant association between the
shared dishes, GI disorders, fatigue and weakness and level of TIBC,
ferritin, Iron and IgG (p < 0.001).
CONCLUSIONS:
The significant relationship between the iron level, IgG titer and H.
pylori infection rate can be referred to as important factors
influencing the anemia rate. Therefore, H. pylori IgG test can be
checked for anemia together with the other routine tests.
PMID: 21526105
PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21526105/?tool=pubmed
And now i see THAT--> A. Khosravi and SK Mazmanian go back to PMID:
21034976
I posted their [PMID: 21034976] abstract on May 20, 2011:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+21034976+&start=0&
here:
Fri, May 20 2011 4:31 pm
Subject: Sarkis K. Mazmanian ---Curing Th2 (Cancer) with GUT BUGs<---
my kinda scientist. --> AS L. Plantarum (Kimchi) cures Th1
(autoimmunity conditions)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/1d28725ebfd3a83c
[...] http://www.ncbi.nlm.nih.gov/pubmed/21034976
Adv Immunol. 2010;107:243-74.
Host-bacterial symbiosis in health and disease.
Chow J, Lee SM, Shen Y, Khosravi A, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena,
California, USA.
Abstract
All animals live in symbiosis. Shaped by eons of co-evolution, host-
bacterial associations have developed into prosperous relationships
creating mechanisms for mutual benefits to both microbe and host. No
better example exists in biology than the astounding numbers of
bacteria harbored by the lower gastrointestinal tract of mammals. The
mammalian gut represents a complex ecosystem consisting of an
extraordinary number of resident commensal bacteria existing in
homeostasis with the host's immune system. Most impressive about this
relationship may be the concept that the host not only tolerates, but
has evolved to require colonization by beneficial microorganisms,
known as commensals, for various aspects of immune development and
function. The microbiota provides critical signals that promote
maturation of immune cells and tissues, leading to protection from
infections by pathogens. Gut bacteria also appear to contribute to non-
infectious immune disorders such as inflammatory bowel disease and
autoimmunity. How the microbiota influences host immune responses is
an active area of research with important implications for human
health. This review synthesizes emerging findings and concepts that
describe the mutualism between the microbiota and mammals,
specifically emphasizing the role of gut bacteria in shaping an immune
response that mediates the balance between health and disease.
Unlocking how beneficial bacteria affect the development of the immune
system may lead to novel and natural therapies based on harnessing the
immunomodulatory properties of the microbiota.
PMID: 21034976
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21034976/?tool=pubmed
READ this AGAIN from that link:
http://7thspace.com/headlines/380215/the_human_gut_is_filled_with_100_trillion_symbiotic_bacteria.html
OK i WILL randall TAR baby...
And i'm sure you will READ it again NOW: LoL
[...] The human gut is filled with 100 trillion symbiotic bacteria—ten
times more microbial cells than our own cells—representing close to
one thousand different species. "And yet, if you were to eat a piece
of chicken with just a few Salmonella, your immune system would mount
a potent inflammatory response," says Sarkis K. Mazmanian, assistant
professor of biology at the California Institute of Technology
(Caltech).
Salmonella and its pathogenic bacterial kin don't look that much
different from the legion of bacteria in our gut that we blissfully
ignore, which raises the question: What decides whether we react or
don't? Researchers have pondered this paradox for decades.
In the case of a common "friendly" gut bacterium, Bacteroides
fragilis, Mazmanian and his colleagues have figured out the surprising
answer: "The decision is not made by us," he says. "It's made by the
bacteria. Since we are their home, they hold the key to our immune
system."
What's more, the bacteria enforce their "decision" by hijacking cells
of the immune system, say Mazmanian and his colleagues, who have
figured out the mechanism by which the bacteria accomplish this feat—
and revealed an explanation for how the immune system distinguishes
between beneficial and pathogenic organisms.
In addition, the work, described in the April 21 issue of Science
Express, "suggests that it's time to reconsider how we define self
versus non-self," Mazmanian says.
Like other commensal gut bacteria—those that provide nutrients and
other benefits to their hosts, without causing harm—B. fragilis was
thought to live within the interior of the gut (the lumen), and thus
far away from the immune system. "The dogma is that the immune system
doesn't respond to symbiotic bacteria because of immunological
ignorance," Mazmanian explains. "If we can't see them, we won't react
to them."
But using a technique called whole-mount confocal microscopy to study
the intestines of mice, he and his colleagues found that the bacteria
actually live in a unique ecological niche, deep within the crypts of
the colon, "and thus in intimate contact with the gut mucosal immune
system," he says.
"The closeness of this association highlights that an active
communication is occurring between the bacteria and their host," says
Caltech postdoctoral scholar June L. Round.
From that vantage point, the bacteria are able to orchestrate control
over the immune system—and, specifically, over the behavior of immune
cells known as regulatory T cells, or Treg cells. The normal function
of Treg cells is to prevent the immune system from reacting against
our own tissues, by shutting down certain immune responses; they
therefore prevent autoimmune reactions (which, when uncontrolled, can
lead to diseases such as multiple sclerosis, type 1 diabetes, lupus,
psoriasis, and Crohn's disease).
Bacteroides fragilis has evolved to produce a molecule that tricks the
immune system into activating Treg cells in the gut, but in this case,
Mazmanian says, "the purpose is to keep the cells from attacking the
bugs. Beautiful, right?"
In their Science paper, Mazmanian and colleagues describe the entire
molecular pathway that produces this effect. It starts with the
bacteria producing a complex sugar molecule called polysaccharide A
(PSA). PSA is sensed by particular receptors, known as Toll-like
receptors, on the surfaces of Treg cells, thus activating those cells
specifically. In response, Treg cells suppress yet another type of
cell, the T helper 17 (Th17) cells. Normally, Th17 cells induce pro-
inflammatory responses—those that would result, for example, in the
elimination of foreign bacteria or other pathogens from the body. By
shutting those cells down, B. fragilis gets a free pass to colonize
the gut. "Up until now, we have thought that triggering of Toll-like
receptors resulted solely in the induction of pathways that eliminate
bacteria," says Round. "However, our studies suggest that multiple yet
undiscovered host pathways allow us to coexist with our microbial
partners."
When Mazmanian and his colleagues blocked this mechanism—by removing
the PSA molecule, by removing the Toll-like receptor for PSA, or by
eliminating the Treg cells themselves—the bacteria were attacked by
the immune system and expelled. "They can no longer co-opt the immune
system into inducing an anti-inflammatory response, so the formerly
benign bacterium now looks like a pathogen," he says, "although the
bug itself is exactly the same."
"Our immune system arose in the face of commensal colonization and
thus likely evolved specialized molecules to recognize good bacteria,"
says Round. Mazmanian suspects that genetic mutations in these
pathways could be responsible for certain types of immune disorders,
including inflammatory bowel disease: "The question is, do patients
get sick because they are rejecting bacteria they shouldn't reject?"
On a more philosophical level, Mazmanian says, the findings suggest
that our concept of "self" should be broadened to include our many
trillions of microbial residents. "These bacteria live inside us for
our entire lives, and they've evolved to look and act like us, as part
of us," he says. "As far as our immune system is concerned, the
molecules made by gut bacteria should be tolerated similarly to our
own molecules. Except in this case, the bacteria 'teaches' us to
tolerate them, for both our benefit and theirs."
<snip>
June Round gets AROUND with Mazmanian:
5 hits:
"Mazmanian SK"[Author] round
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mazmanian%20SK%22%5BAuthor%5D%20round
I havent' posted these two:
#3 of 5
http://www.ncbi.nlm.nih.gov/pubmed/19963349
J Autoimmun. 2010 May;34(3):J220-5. Epub 2009 Dec 6.
Coordination of tolerogenic immune responses by the commensal
microbiota.
Round JL, O'Connell RM, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, 1200 E.
California Blvd, Pasadena, CA, USA. jro...@caltech.edu
Abstract
All mammals are born ignorant to the existence of micro-organisms.
Soon after birth, however, every mammal begins a lifelong association
with a multitude of microbes that lay residence on the skin, mouth,
vaginal mucosa and gastrointestinal (GI) tract. Approximately 500-1000
different species of microbes have highly evolved to occupy these
bodily niches, with the highest density and diversity occurring within
the intestine. These organisms play a vital role in mammalian nutrient
breakdown and provide resistance to colonization by pathogenic micro-
organisms. More recently, however, studies have demonstrated that the
microbiota can have a profound and long-lasting effect on the
development of our immune system both inside and outside the
intestine. While our immune system has evolved to recognize and
eradicate foreign entities, it tolerates the symbiotic micro-organisms
of the intestine. How and why this tolerance occurs has remained
unclear. Here we present evidence that the commensal microbes of the
intestine actively induce tolerant responses from the host that
coordinate healthy immune responses. Potentially, disruption of this
dialogue between the host and microbe can lead to the development of
autoimmune diseases such as inflammatory bowel disease (IBD),
rheumatoid arthritis (RA), or Type I diabetes (TID). As a wealth of
publications have focused on the impact of the microbiota on
intestinal immune responses and IBD, this chapter will focus on the
extra-intestinal impacts of the microbiota from development to disease
and integrate the known mechanisms by which the microbiota is able to
actively communicate with its host to promote health.
PMID: 19963349
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19963349/?tool=pubmed
#4 of 5
http://www.ncbi.nlm.nih.gov/pubmed/19343057
The gut microbiota shapes intestinal immune responses during health
and disease.
Round JL, Mazmanian SK.
Nat Rev Immunol. 2009 May;9(5):313-23. Review. Erratum in: Nat Rev
Immunol. 2009 Aug;9(8):600.
PMID: 19343057
^^^^^^^^^^^^^^^^^^^^^^
And we have 26 hits for MUC1 in the group as of today:
muc1 - 26 hits - P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=muc1&start=0&
ONLY 3 of these 26 have iron... till today of course:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=muc1+iron+&start=0&
ONLY 47 muc1 + iron in ALL groups:
http://groups.google.com/groups/search?qt_s=1&q=muc1+iron+
And a clue from one of them takes me HERE:]
http://www.cancer.gov/cancertopics/pdq/cam/laetrile/HealthProfessional/page4
[...] In the fourth study, cultured human bladder cancer cells were
treated with amygdalin alone or a combination of amygdalin and an
antibody that was coupled (chemically) to beta-glucosidase.[20] The
target for this antibody was the glycoprotein (a protein with sugar
molecules attached) MUC1. Aberrant forms of MUC1 are produced and
displayed at high levels on the outside of several types of cancer
cells, including bladder cancer cells. In this study, amygdalin alone
was not very effective in killing the bladder cancer cells, but its
cell-killing ability was 36 times greater in the presence of the
antibody-enzyme complex. There are two possible explanations for this
increase in cell-killing ability. The first is that antibody-enzyme
complexes bound via MUC1 produce high rates of amygdalin breakdown at
the cell surface. This breakdown leads to high local production of
cyanide, which is quickly taken up by the cells and kills them. The
second explanation is that antibody-enzyme complexes bound to the
cells are internalized, thereby increasing the intracellular
concentration of beta-glucosidase. Increased beta-glucosidase activity
inside a cell would result in increased breakdown of amygdalin taken
up by it, and increased cyanide production and cell death. These two
potential mechanisms are not mutually exclusive. In another
experiment, the researchers cultured bladder cancer cells in the
presence of human brain tumor cells, which do not express MUC1. When
this coculture was treated with amygdalin and the antibody-enzyme
complex, the bladder cancer cells were killed selectively. In view of
the mechanisms proposed above, this result is not surprising, since
the bladder cancer cells and the brain tumor cells in this coculture
formed homogeneous colonies (colonies that contained exclusively
bladder cancer cells or brain tumor cells). Conceivably, selective
killing of some types of human cancer cells might be achievable
through application of this method; however, these positive results
must be confirmed independently, and the effectiveness of this
approach in animal models must be demonstrated before its use in
humans can be considered.
<snip>
Eat soybeans and take a chill pill?
http://www.ncbi.nlm.nih.gov/pubmed/21593350
Soy protein diet, but not Lactobacillus rhamnosus GG, decreases
mucin-1, trefoil factor-3, and tumor necrosis factor-α in colon of
dextran sodium sulfate-treated C57BL/6 mice.
Jiang H, Przybyszewski J, Mitra D, Becker C, Brehm-Stecher B,
Tentinger A, MacDonald RS.
J Nutr. 2011 Jul;141(7):1239-46. Epub 2011 May 18.
PMID: 21593350
^^^^^^^^^^^^^^^^^^^^^^^^
Little-Known Secrets about Optimal Iron Levels
Posted By Dr. Mercola | July 14 2009
http://articles.mercola.com/sites/articles/archive/2009/07/14/Little-Known-Secrets-about-Optimal-Iron-Levels.aspx
[...] mercola -Is Iron Helping or Slowly Killing You?
http://www.youtube.com/watch?v=g8pQsH7c1sc
<time: 8:44> <views: 3,675>
=================
Build uP GpX and SOD via Glutathione and NAC supplements:
http://www.whale.to/vaccine/tylenol_depletes_glutathione.html
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
randall... i better get some eXXXercise... now... i want HIGHer IRON
(Fe) levels to be strongER
Are you FAT becaUSE YOU eat twinkies all day LONG?
Should obamacare allow obese people to get pregnant if your chance of
having an autistic child is
in 55 or higher due to low glutathione (NAC) levels?
Should you be allowed to take tyelenol (Acetaminophen), which lower's
GLUTATHIONE (NAC), if pregnant?
And what about being and eating IRON?
Certainly women have a monthly release valve on iron....
Should obamacare order men to have a period to give blood
and thereby lower IRON levels? To EVEN things OUT?
Should women have to take testosterone after menopause then?
What will obamaCARE care about? You, me or the goons of gov run by
goonunions:
http://www.hillsdale.edu/images/userImages/mvanderwei/Page_6907/Imprimis_March12.pdf
What Public Employee Unions are Doing to Our Country
William McGurn
<snip>
Is goonulism due to excess iron (red meat) in their diets? How do we
put the gov on a DIET?
OTOH (on the other HAM.... easter you know... LOL)
What if your iron is already to LOW due to being a VEGAN perhaPs?
But, but, but.... LANCE ARMSTRONG is vegan : NOW:
http://www.ecorazzi.com/2012/04/09/lance-armstrong-fuels-fitness-with-a-mostly-vegan-diet/
How does he suPPlement to keep his minerals optimum?
------------------------------------
IRON MAN & Women ALERT...... not Robert Downey or Gwyneth Paltrow...
of course...
Iron IS in the FIREs of LIfE?
Who KNEW low iron is caused by excess INFLAMMATION?
REALLY... no...REALLY?
WHO SAID so?
Byron KNOWs in the next article:
Psor people are full of inflammation and the more severe the wORSE it
is...
Hey! Don't BE severe!
:(
Yikes... i've got it.... how do i stoPPer it?
er er er...?
And with NO to LOW--> ENERGY in me MITO's..... yikes..
STAT to the ER and fity grams of Fe for me?
From: BYRON Today:
http://www.wellnessresources.com/weight/articles/stunning_discoveries_regarding_iron_obesity_candida_thyroid/
Stunning Discoveries Regarding Iron, Obesity, Candida & Thyroid
Friday, April 06, 2012 - Byron Richards
The information contained in this groundbreaking article applies to at
least 75 percent of people who are struggling to lose weight. It is a
major factor contributing to the fatigue associated with being
overweight and having symptoms of hypothyroid. It involves new
discoveries regarding iron metabolism and explains why even if you eat
plenty of iron you may still have rather dramatic iron deficiency
issues, which handicap your metabolism and thyroid function.
Traditional thinking about iron is that either you get enough in your
diet or you don’t. People who don’t eat red meat, menstruating women,
those who exercise a lot, and those with digestive bleeding or other
blood loss issues are at risk for iron deficiency, and either
functional or blatant anemia. In general, iron deficiency is thought
to be associated with undernutrition or malnourished states.
Ironically, in the past few years, it has become clear that at least
half the people who are overweight have impaired iron metabolism
detectable on blood tests. In many of these cases dietary iron intake
was adequate, perplexing researchers. It now appears that the
inflammation associated with being overweight is elevating a hormone
in your liver called hepcidin, which has the net effect of reducing
iron absorption into your body from your digestive tract. The net
result is a metabolic nightmare of weight gain, fatigue, and poor
thyroid function.
Hepcidin 101
Hepcidin is a hormone produced in your liver, discovered in the year
2000. Scientists have discovered that it regulates iron use
throughout your body (iron homeostasis). One of the ways hepcidin
regulates your iron status is by deciding how much iron to let in to
your body. In essence it communicates directly to the cells of your
digestive tract, either allowing them or not allowing them to let iron
in. High levels of hepcidin reduce or prevent dietary iron intake
into your body, regardless of the iron content of your food.
It is now clear that hepcidin levels elevate in response to
inflammation. This could be from inflammation of any type: infection,
toxin exposure, excess alcohol, many medications, injury, excess
exercise, lack of sleep, too much stress, etc. In this regard, being
overweight is an ongoing inflammatory problem wherein your extra
pounds of white adipose tissue crank out inflammatory signals 24 hours
a day, 7 days a week, as if someone will not stop yelling at you. The
more excess weight you have, the higher the inflammation (in addition
to all other potential sources of inflammation).
Iron is utterly indispensable to your metabolism and survival. For
example, mice that are genetically bred to have high levels of
hepcidin die within a few days from iron deficiency. Iron is need for
growth, repair, assembly of proteins into your body structures, the
function of your nerves, and much more.
On the other hand, iron is highly reactive. Your body literally keeps
it in cages like ferritin, kind of like a lion at the zoo. When it is
needed, the lion is let out at the proper place and time so that it
can do something useful. If the cage is opened at the wrong time or
place then iron can jump out and set off free radical chain reactions
that can be very damaging to health. It appears that hepcidin
intentionally reduces iron intake during times of inflammatory stress
to prevent the inflammation from damaging iron transport and storage
systems (causing inappropriate iron release). In other words, if your
body is in a state of inflammatory wear and tear it may be difficult
to use iron in a healthy way.
This would offer excellent survival features for short term
inflammatory distress that are threats to survival. However, a
chronically inflamed person, as from obesity, can develop a real
catch-22 wherein hepcidin is elevated for too long, which creates a
scenario of ongoing iron deficiency, either functional (meaning not
enough iron for metabolism to function well) or blatant (meaning
anemia).
Due to the rampant overuse of antibiotics and high sugar diets of many
people there is an epidemic of Candida albicans overgrowth in
overweight people. This is especially common in overweight people
with thyroid problems, as I have observed first hand for the past 27
years. Interestingly, hepcidin is a powerful antifungal. This means
that your body may raise its hepcidin levels to prevent Candida from
infiltrating your body, which is part of a natural defense system.
Again, this has survival advantages especially in olden times.
However, in a population of people who are overweight and have an
overgrowth of antibiotic-induced Candida, it is a double whammy
against a functioning metabolism.
The Impact of Low Iron on Metabolism
A new study details the dire metabolic consequences of having low
iron. It shows that low iron turns on genes in your liver and muscles
that promote fat storage and cause abnormal elevation of blood sugar –
exactly what goes wrong with metabolism that leads to the metabolic
syndrome.
The consequence to thyroid metabolism is twofold. First, the inactive
thyroid hormone,T4, is converted to the biologically active
hormone,T3, mostly on cell membranes of liver cells. Hepcidin is made
in your liver and is being produced excessively in response to high
inflammation. Such inflammation will also damage liver cell
membranes, thus reducing the conversion of T4 to T3. This is one main
reason why inflammation of any type disturbs thyroid function.
Second, when biologically active thyroid, T3, binds on to cell
membranes and communicates to the nucleus of your cells how fast their
metabolic pace should be set, it is like a hormone manager giving an
order to a cell factory. The worker bees in the cell factory then
need iron for the genes that will implement the thyroid order. In
fact, the next 80 metabolic genes responding to a thyroid order all
need iron. If iron is lacking metabolism simply cannot run at an
optimal pace, which will give a person all the symptoms of hypothyroid
even if they have normal T4 and normal T3.
Iron can be normal on a blood test and a person can still have all the
problems above, though levels tend to be toward the lower end of the
normal range. Hemoglobin (Hgb) and hematocrit (Hct) are also on the
low side of the normal range with this problem. If one or another is
out of range on the low side it signifies a major problem. Serum
ferritin is typically low or low normal, unless inflammation is very
high, which can actually drive up ferritin scores. Lab tests can
help, however, fatigue along with trouble losing weight despite eating
better and exercising are general indicators of a potential problem.
Solving Iron Deficiency relating to Stubborn Weight
Adequate iron intake (red meat) compared to obvious iron loss
(menstrual cycles, etc.) is still important to understand. However,
this new data says that a condition of less inflammation must exist in
order for iron to work properly in your body.
The most basic approach is to follow The Leptin Diet, which is anti-
inflammatory. As you begin to lose weight you are now reducing
inflammation, hepcidin levels should come down, and the iron in your
diet will work better. If you have little iron in your diet, then you
should take a high quality iron supplement. I like iron glycinate, a
true protein chelate of iron. I would stay away from all cheap iron
salts, such as ferrous sulfate (these cause free radical damage).
In reality there are many basic supplements that are fundamental to
metabolism along with a good diet, as I have outlined in The Leptin
Diet Weight Loss Challenge #1 – Overview and Basic Needs. All of
these are important to contribute to anti-inflammatory basic
nutrition. Based on the new information in this article, it is
accurate to say that ensuring you have adequate iron intake should be
added to this basic list of nutrient needs for weight loss, especially
in conjunction with basic anti-inflammatory nutrition.
A more comprehensive approach to this specific issue is to take an
iron supplement as a trial to see if it helps your energy.
Additionally, fat-soluble antioxidants that are targeted to improve
liver function would be top choices. My top recommendations would be
acetyl-l-carnitine, coenzyme Q10, tocotrienol E, r-alpha lipoic acid,
and silymarin. Many other anti-inflammatory nutrients may also be of
value. Your bottom line is to get enough support to engage the
process of weight loss, maintain steady progress, have a much better
energy level, and on a blood test your hemoglobin and hematocrit
should be in the middle of the normal range.
Some individuals may need to employ a more targeted anti-Candida
program to fully solve this problem. I discuss these topics more
fully in my series of comprehensive articles on the Leptin Diet Weight
Loss Challenge. It is important to know the direction you are
heading. If you are doing well and making progress then you are most
likely doing enough – at least as long as you are getting somewhere.
If you hit a plateau or fail to get out of the starting block then you
certainly need to become an active problem solver for your metabolic
issues. Hepcidin issues are far more common than not in any person
who struggles with weight.
Summary
Your body handles iron as a top priority, since it is vital to
survival as well as being potentially problematic. Iron is essential
for metabolism to run properly, including normal thyroid activation
and cellular function. The inflammation of obesity is elevating a
hormone called hepcidin, which has the unfortunate side effect of
disrupting iron metabolism in your body. This mechanism helps you
overcome short term inflammation and was very handy in olden times for
survival purposes. In modern times, especially in a population of
overweight people who often have Candida issues, it can viciously lock
in place malfunctioning metabolism. Solving the problem requires
adequate iron intake along with a reduction in inflammation. Reducing
life stress helps. Sleeping better helps. Following The Leptin Diet
helps. Many dietary supplements can also help reduce inflammation.
Especially important may be the fat-soluble antioxidants that help
reduce liver inflammation, the place of hepcidin synthesis. Use
enough support to feel a difference in your energy level while
engaging and sustaining the process of healthy weight loss. There is
a path to a healthier you!
<snip>
------------
24 hits for mito DNA - p ng
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=mitochondrial+dna&start=0&
Is one of 24 the clue for fatigue?
Why Autoimmune people are so depressed is ER?
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/c2686d542d831738/31051264331a0bc7?lnk=gst&q=mitochondrial+dna#31051264331a0bc7
So give some credit to : Ward Dean, M.D., and Steven Wm. Fowkes
http://www.ceri.com/mito.htm
<from: psors1rnaDNAsilencing>
--------------
^^^^^^^^^^^^^^^^^^^^^^^^
Touch ME now...
The Doors - Touch Me
http://www.youtube.com/watch?v=4UEVyIyibD8
http://www.vrp.com/stress/take-on-anxiety-with-the-power-of-touch?utm_content=article3511
TAKE ON ANXIETY WITH THE POWER OF TOUCH
A grueling commute, a high-pressure job, a shrinking 401K or mounting
family demands… when you’re burning the candle at both ends, it may
seem like the only way to escape the chaos is a one-way ticket to the
nearest private island. But what if you could get a break from the
daily onslaught of stress without packing a single bag?
As it turns out, a permanent vacation isn’t the only way to give your
mind and body some much needed respite. A growing body of research
shows that an alternative therapy called reflexology may also be an
effective antidote to health-robbing anxiety.
The Healing “Zone”
So what is reflexology, exactly?
Well, similar to practices like acupressure and acupuncture,
reflexology relies upon a complex map of designated points on the
hands, feet and ears—so-called “zones” or “reflex points”—that
correspond to various organs and systems in your body.
According to the principles of reflexology, applying purposeful
pressure to these specific points can help to balance the body’s
energy and affect the function of corresponding systems, yielding
powerful therapeutic effects—such as pain relief, increased energy
and, of course, anxiety reduction.
As a healing method, reflexology has enjoyed a long history, appearing
in records as far back as ancient Egypt. Its first introduction in the
United States dates back to the early 20th century—but even modern
science supports its use in dealing with everyday maladies, with
published studies pointing to the effectiveness of reflexology when
used by itself or as part of a larger complementary health strategy.
Mind-Body Stress Relief… and More
In a pilot study published in January 2004, 30 healthy subjects
received either reflexology or no treatment, with the latter group
serving as a control. Researchers assessed each participant for self-
reported anxiety, stress-related heart parameters (including blood
pressure and heart rate) and salivary levels of cortisol and melatonin—
two hormones directly involved in the body’s stress response—both
before and after the reflexology treatments.
Results showed that reflexology had powerful anti-anxiety benefits,
reducing both anxious states in the subjects, as well as blood
pressure and heart rates.1 In fact, the outcome was promising enough
that the researchers intend to transfer their findings to a new study
involving women with breast cancer—a circumstance under which
reflexology’s stress-modulating effects may be particularly
pronounced, due to the prevalence of cortisol and melatonin imbalances
in these patients.
In the meantime, the potential benefit of this calming natural cure is
clear. Considering the dangerous link between chronic stress and a
long list of serious health problems—from reduced immunity and
increased inflammation to higher risk of heart disease and cancer—it’s
easy to see how reflexology could end up playing a vital role in
therapeutic protocols for any number of conditions.
It’s also no surprise that published research already backs up
reflexology as a drug-free form of relief for anything from menstrual
pain, backache and constipation to fibromyalgia and even Parkinson’s
disease.2-6
To find a qualified reflexology therapist in your area, you can
perform a simple search through the Reflexology Association of
America. Your frazzled nerves will thank you for it.
References:
<snip>
^^^^^^^^^^^^^^^^^^^
Isn't this next one predicated on levels of iron and iodine etc?
Or selling some genetic analysis?
23andMe identifies 5 significant genetic associations for
hypothyroidism
April 9, 2012 in Genetics
Using its unique online research platform, 23andMe, a leading personal
genetics company, has found five significant genetic associations for
hypothyroidism in the largest known genome-wide association study of
hypothyroidism conducted to date. The details of the study are now
available online in the journal PLoS ONE.
"With nearly 90 percent of our 125,000 customers participating in our
online research, 23andMe is making crowd-sourced science a reality,"
stated 23andMe CEO and co-founder Anne Wojcicki. "Our online research
platform continues to advance research faster and more cost
effectively than traditional research models," added Wojcicki.
Of the five significant associations reported in this study, three are
known to be involved in other autoimmune diseases. These include
rs6679677 near PTPN22, rs3184504 in SH2B3, and rs2517532 in the HLA
class I region. The other two associations reported here are rs4915077
near VAV3 and rs925489 near FOXE1, a gene involved in thyroid
development. In addition, 23andMe observed associations with two loci
marginally associated with hypothyroidism that have been linked to
Thyroid Stimulating Hormone (TSH) levels, PDE8B and CAPZB as well as
another gene previously associated with hypothyroidism and autoimmune
disease (CTLA4).
"These genetic associations contribute significantly to understanding
the underlying biology of hypothyroidism, which impacts five percent
of the general population," remarked 23andMe Medical Director and
study co-author Dr. Uta Francke. "Identification of associations with
other autoimmune disorders opens up potential pathways of treatment."
Upon identification of those novel genetic associations for
hypothyroidism also associated with autoimmune diseases, the 23andMe
research team looked for any additional single-nucleotide
polymorphisms (SNPs) shared with other autoimmune diseases,
investigating a list of 107 SNPs that were studied across seven
autoimmune diseases. Among this list, only the CTLA4, PTPN22, and
SH2B3 loci show significant association with hypothyroidism.
According to 23andMe Principle Scientist and Lead Author Nicholas
Eriksson, Ph.D., "These findings shed new light on the biology of
hypothyroidism, showing that genes involved with both thyroid function
and immune response impact this disease. This demonstrates our ability
to harness the power of the enormous 23andMe genetic database to
further medical research.
This study investigated 3,736 individuals with hypothyroidism as well
as 35,546 controls, all drawn from the more than 100,000 23andMe
customers who have consented to participate in research efforts. Cases
included individuals who have been diagnosed with hypothyroidism, have
elevated TSH levels, or are taking thyroid hormone replacement
medication.
These results continue to validate 23andMe's methodology in combining
self-reported data on phenotypes gathered via web-based questionnaires
and genotypic data derived from self-collected saliva samples. 23andMe
had previously published its first proof-of-concept results in the
journal PLoS Genetics in June 2010 which reported novel associations
for unusual traits such as asparagus anosmia and photic sneeze reflex
and replicated associations for other common genetic traits, and
recently published the discovery of two novel genetic associations for
Parkinson's disease in PLoS Genetics, and presented a major
replication study of over 180 genetic associations in the journal PLoS
ONE in August 2011.
<snip>
^^^^^^^^^^^^^^^^^^
THE
"OCCUPY GOLF" MOVEMENT
WE NEED TO BE HEARD!!!
I am a member of golf ’ s lower 99%.
I am an indifferent golfer,
there i s no way I could ever make it
to the professional level.
I will never put in the practice
Time to be the best.
I will never have the shots,
skills, or mental toughness
to make it in the sport.
I just never felt like working
all that hard at it.
However,
I am a part of the
golfing community,
as such,
feel I should be paid
by the top 1% of golfers
for what I do.
It isn't fair that those players
who have worked harder,
have studied the game
more carefully,
have better equipment,
are more skilled and dedicated
should make all that BIG money.
Where's my share?
I a m a Victim!
The top 1% should pay for
my club memberships
and green fees and lessons,
buy me new clubs, balls,
clothes and shoes, and
pay me some of their winnings.
They can afford it.
They are The Rich .
The whole system should be changed
to accommodate people like me.
I think we should get together
and "occupy" a golf course;
demand that those who are
better at what they do,
pay for us who generally suck.
Whining should get us something -
maybe we'll make the cover of
Time Magazine
And garnish some public sympathy.
Hell, during this election year,
we may even get a law or two
passed by legislators who want
our votes.
The "Occupy Golf "Movement
P.S. – Don ’ t mention this to tennis players!
We thought of it first!!!
We are planning to occupy the front
of the gate at the Masters this year.
remember i t’s for the 99%.
Bring your signs
^^^^^^^^^^^^^^^^^^^^^^^
And if you can't relax and have zero energy and risk getting cancer
as your gut microbiota are funky.... then fix the muck gene.
Muc1 <<mucins and mucus in your Gi TRACT-- think pancan and black
cohosh?>>
see
http://en.wikipedia.org/wiki/MUC1
http://www.dailymail.co.uk/health/article-2127238/Universal-vaccine-tackle-90-cent-cancers-tested-humans-time.html
'Universal' vaccine that could beat 90 per cent of cancers is tested
on humans for first time
Vaccine triggered greater immunity to cancer cells in trial patients
By FIONA MACRAE and CLAIRE BATES
UPDATED: 08:44 EST, 9 April 2012
A vaccine that targets a molecule in 90 per cent of all cancers has
been tested on humans for the first time.
Results from the safety trial - on patients with blood cancer - found
all had greater immunity to the disease after receiving the vaccine.
Three of the seven patients who have completed the treatment are now
free of the condition.
As a therapeutic vaccine it is designed to be given to patients to
help their bodies fight cancer rather than the majority - known as
prophylactic vaccines - that aim to prevent disease in the first
place.
Researchers believe the jab could also tackle breast, prostate,
pancreatic, bowel and ovarian cancers
Even tumours that resist treatment with the best medicines on the
market, including the breast cancer ‘wonder drug’ Herceptin, may be
susceptible to the vaccine.
If all goes well, the vaccine – called ImMucin – could be on the
market by 2020.More than 300,000 cases of cancer are diagnosed in
Britain each year and the disease kills around half this number
annually.
Rather than attacking cancer cells, like many drugs, the new treatment
harnesses the power of the immune system to fight tumours.
The search for cancer vaccines has until now been hampered by fears
that healthy tissue would be destroyed with tumours.
Researchers from the drug company Vaxil Biotheraputics and Tel Aviv
University have focused on a protein called MUC1 that is made in
bigger amounts in cancerous cells than in healthy ones.
Not only is there more of it, but a sugar that it is ‘decorated’ with
has a distinctive shape.
The vaccine ‘trains’ the immune system to recognise the rogue sugar
and turn its arsenal against the cancer.
The misshaped MUC1 sugar is found in 90 per cent of all cancers. There
have been ‘dramatic’ results in tests on mice with breast tumours.
Now, Vaxil Biotheraputics have announced promising results in a human
safety trial.
Ten patients suffering from multiple myeloma, a form of blood cancer,
have now received the vaccine received the vaccine at the Hadassah
Medical Centre in Jerusalem.
Seven of the patients have finished the treatment and Vaxil reported
that all of them had greater immunity against cancer cells compared to
before they were given the vaccine. Of the seven, three patients are
reportedly free of detectable cancer.
None of them have reported suffering side-effects apart from minor
irritation.
A statement from Vaxil Biotheraputics said: 'ImMucin generated a
robust and specific immune response in all patients which was observed
after only 2-4 doses of the vaccine out of a maximum of 12 doses.
'In some of the patients, preliminary signs of clinical efficacy were
observed.'
Years of large-scale human trials will be needed before the drug is
judged safe and effective for widespread use in hospitals.
It could then be used with existing drugs to boost treatment and given
to prevent tumours from coming back after surgery.
Men and women known to be at high risk of cancer because of their
genes could also be vaccinated in an attempt to stop tumours from
appearing.
Dr Caitlin Palframan, of Breakthrough Breast Cancer, said: ‘This
exciting new approach could lead to treatments for breast cancer
patients who have few options.
‘It also opens up the possibility of vaccinating high-risk women
against breast cancer in the future.'
<snip>
http://en.wikipedia.org/wiki/MUC1
Mucin 1, cell surface associated (MUC1) or polymorphic epithelial
mucin (PEM) is a mucin encoded by the MUC1 gene in humans.[1] MUC1 is
a glycoprotein with extensive O-linked glycosylation of its
extracellular domain. Mucins line the apical surface of epithelial
cells in the lungs, stomach, intestines, eyes and several other organs.
[2] Mucins protect the body from infection by pathogen binding to
oligosaccharides in the extracellular domain, preventing the pathogen
from reaching the cell surface.[3] Overexpression of MUC1 is often
associated with colon, breast, ovarian, lung and pancreatic cancers
[...] Role in Cancer
The ability of chemotherapeutic drugs to access the cancer cells is
inhibited by the heavy glycosylation in the extracellular domain of
MUC1. The glycosylation creates a highly hydrophilic region which
prevents hydrophobic chemotherapeutic drugs from passing through. This
prevents the drugs from reaching their targets which usually reside
within the cell. Similarly, the glycosylation has been shown to bind
to growth factors. This allows cancer cells which produce a large
amount of MUC1 to concentrate growth factors near their receptors,
increasing receptor activity and the growth of cancer cells. MUC1 also
prevents the interaction of immune cells with receptors on the cancer
cell surface through steric hindrance. This inhibits an anti-tumor
immune response.[2]
Preventing Cell Death
MUC1 cytoplasmic tail has been shown to bind to p53. This interaction
is increased by genotoxic stress. MUC1 and p53 were found to be
associated with the p53 response element of the p21 gene promoter.
This results in activation of p21 which results in cell cycle arrest.
Association of MUC1 with p53 in cancer results in inhibition of p53-
mediated apoptosis and promotion of p53-mediated cell cycle arrest.
[17]
Overexpression of MUC1 in fibroblasts increased the phosphorylation of
Akt. Phosphorylation of Akt results in phosphorylation of Bcl-2-
associated death promoter. This results in dissociation of Bcl-2-
associated death promoter with Bcl-2 and Bcl-xL. Activation was shown
to be dependent on the upstream activation of PI3K. Additionally, MUC1
was shown to increase expression of Bcl-xL. Overexpression of of MUC1
in cancer. The presence of free Bcl-2 and Bcl-xL prevents the release
of cytochrome c from mitochondria, thereby preventing apoptosis.[18]
MUC1 cytoplasmic tail is shuttled to the mitochondria through
interaction with hsp90. This interaction is induced through
phosphorylation of the MUC1 cytoplasmic tail by Src (gene). Src is
activated by the EGF receptor family ligand Neuregulin. The
cytoplasmic tail is then inserted into the mitochondrial outer
membrane. Localization of MUC1 to the mitochondria prevents the
activation of apoptotic mechanisms.[19]
Promoting Tumor Invasion
MUC1 cytoplasmic tail was shown to interact with Beta-catenin. A
SXXXXXSSL motif was identified in MUC1 that is conserved with other
beta-catenin binding partners. This interaction was shown to be
dependent on cell adhesion.[20] Studies have demonstrated that MUC1 is
phosphorylated on a YEKV motif. Phosphorylation of this site has been
demonstrated by LYN through mediation of interleukin 7,[21] Src
through mediation of EGFR,[22][23] and PRKCD.[24] This interaction is
antagonized by degradation of beta-catenin by GSK3B. MUC1 blocks the
phosphorylation-dependent degradation of beta-catenin by GSK3B.[25]
[26] The end result is that increased expression of MUC1 in cancer
increases stabilized beta-catenin. This promotes the expression of
vimentin and CDH2. These proteins are associated with a mesenchymal
phenotype, characterized by increased motility and invasiveness. In
cancer cells, increased expression of MUC1 promotes cancer cell
invasion through beta-catenin, resulting in the initiation of
epithelial-mesenchymal transition which promotes the formation of
metastases
<snip>
8 hits: iron muc1 -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=muc1%20iron
1941 hits : muc1 cancer
http://www.ncbi.nlm.nih.gov/pubmed?term=muc1%20cancer
20 hits: mucin FRAGILIS - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=mucin%20fragilis
<note: zero hit: fragilis muc1 etc>
And #2 of 20 being so KEY.....to me anyWHEY...
http://www.ncbi.nlm.nih.gov/pubmed/21664470
The human commensal Bacteroides fragilis binds intestinal mucin.
Huang JY, Lee SM, Mazmanian SK.
Anaerobe. 2011 Aug;17(4):137-41. Epub 2011 Jun 2.
PMID: 21664470
And since Sarkis is my FAVORITE due to fragilis binding...s
Then we look at his most recent...
And no MEAT in the taco.... Bummer ...
http://www.ncbi.nlm.nih.gov/pubmed/22481405
Nat Med. 2012 Apr 5;18(4):492-4. doi: 10.1038/nm.2723.
Breathe easy: microbes protect from allergies.
Khosravi A, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena,
California, USA.
PMID: 22481405
Since i know what SK is doing...we look at
80 hits: "Khosravi A"[Author] -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Khosravi%20A%22%5BAuthor%5D
The ONE that caught my attention
#8 of 80
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22291830/?tool=pubmed
http://www.ncbi.nlm.nih.gov/pubmed/22291830
Arch Med Sci. 2011 Oct;7(5):844-9. Epub 2011 Nov 8.
Evaluation of Helicobacter pylori infection in patients with common
migraine headache.
Hosseinzadeh M, Khosravi A, Saki K, Ranjbar R.
Source
Department of Immunology, Faculty of Medicine, Ilam University of
Medical Sciences, Ilam, Iran.
Abstract
INTRODUCTION:
Migraine can cause headache in different communities so that 12-15%
are suffering worldwide. Recently the relationship between infectious
diseases such as Helicobacter pylori infection and migraine headache
has been the focus of many studies. The current study was designed to
evaluate IgG and IgM antibodies to H. pylori in patients suffering
from migraine headaches.
MATERIAL AND METHODS:
Patients who had diagnostic criteria for migraine were chosen as cases
compared to some healthy individuals as the control group amongst
which immunoglobulin G (IgG), immunoglobulin M (IgM), age, job, gastro-
intestinal (GI) disorders, history of migraine, special meals,
medications, sleeping disorders, stress, environmental factors etc
were analysed.
RESULTS:
The prevalence of disease was 38.6%. Household women had the highest
prevalence (40%). Among them menstruation was related to high
prevalence of migraine. 75.6% of patients had gastrointestinal
disorders of which the gastric reflux was the most important sign
(47.1%). The mean optical density (OD) value of IgG and IgM antibody
to H. pylori was 60.08 ±7.7 and 32.1 ±8.7 for the case group, 21.82
±6.2 and 17.6 ±9.4 for the control group, respectively.
CONCLUSIONS:
There was a significant difference in mean OD value of both antibodies
to H. pylori amongst the case and control groups. As a result, active
H. pylori infection is strongly related to the outbreak and severity
of migraine headaches, and H. pylori treatment reduces migraine
headaches significantly. Hopefully, the definite treatment and
eradication of this infection can cure or reduce the severity and
course of migraine headaches significantly if not totally.
PMID: 22291830
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22291830/?tool=pubmed
#20 of 80 helps give a GUT perspective on IRON and what hepcidin Byron
in the first article
tells US.
http://www.ncbi.nlm.nih.gov/pubmed/21526105
J Res Med Sci. 2010 Nov;15(6):324-30.
The antibody titers to Helicobacter pylori in 7 - 12 year old iron
deficiency anemic children, in Ilam.
Hoseinzadeh M, Khosravi A, Sayemiri K, Rasoli MH, Mohaveri A.
Source
Immunology, Ilam University of Medical Sciences, Ilam, Iran.
Abstract
BACKGROUND:
It has recently been revealed that H. pylori infection is one the most
important causes of anemia inhibiting iron uptake. The current study
was designed to evaluate the correlation between the iron deficiency
anemia and IgG to H. pylori in anemic children.
METHODS:
In this analytical study, 100 anemic children were analyzed using
total Iron, Ferritin, TIBC and H. pylori IgG assay. Data were
collected using a questionnaire including parameters of age, blood
group, infancy nutrition, iron consumption, fatigue, weakness, height,
weight, gastrointestinal infectious, parasitic and blood diseases,
parent literacy, income, inhabitation, etc. Data were analyzed using
Multivariate Regression Analysis Models, Pearson Correlation- test and
Kolmogrov Smirnov.
RESULTS:
The most prevalent blood group detected in the study sample was group
O (62%); 79% were breastfed, 9% were bottle- fed, 12% were both
breastfed and bottle- fed. The history of gastrointestinal disorders
was mentioned amongst 91% of the patients' family members. A
significant relationship was observed between the iron level with
serum, ferritin, level of TIBC and elevated level of IgG titer to H.
pylori (p < 0.001). There was a significant association between the
shared dishes, GI disorders, fatigue and weakness and level of TIBC,
ferritin, Iron and IgG (p < 0.001).
CONCLUSIONS:
The significant relationship between the iron level, IgG titer and H.
pylori infection rate can be referred to as important factors
influencing the anemia rate. Therefore, H. pylori IgG test can be
checked for anemia together with the other routine tests.
PMID: 21526105
PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21526105/?tool=pubmed
And now i see THAT--> A. Khosravi and SK Mazmanian go back to PMID:
21034976
I posted their [PMID: 21034976] abstract on May 20, 2011:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+21034976+&start=0&
here:
Fri, May 20 2011 4:31 pm
Subject: Sarkis K. Mazmanian ---Curing Th2 (Cancer) with GUT BUGs<---
my kinda scientist. --> AS L. Plantarum (Kimchi) cures Th1
(autoimmunity conditions)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/1d28725ebfd3a83c
[...] http://www.ncbi.nlm.nih.gov/pubmed/21034976
Adv Immunol. 2010;107:243-74.
Host-bacterial symbiosis in health and disease.
Chow J, Lee SM, Shen Y, Khosravi A, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, Pasadena,
California, USA.
Abstract
All animals live in symbiosis. Shaped by eons of co-evolution, host-
bacterial associations have developed into prosperous relationships
creating mechanisms for mutual benefits to both microbe and host. No
better example exists in biology than the astounding numbers of
bacteria harbored by the lower gastrointestinal tract of mammals. The
mammalian gut represents a complex ecosystem consisting of an
extraordinary number of resident commensal bacteria existing in
homeostasis with the host's immune system. Most impressive about this
relationship may be the concept that the host not only tolerates, but
has evolved to require colonization by beneficial microorganisms,
known as commensals, for various aspects of immune development and
function. The microbiota provides critical signals that promote
maturation of immune cells and tissues, leading to protection from
infections by pathogens. Gut bacteria also appear to contribute to non-
infectious immune disorders such as inflammatory bowel disease and
autoimmunity. How the microbiota influences host immune responses is
an active area of research with important implications for human
health. This review synthesizes emerging findings and concepts that
describe the mutualism between the microbiota and mammals,
specifically emphasizing the role of gut bacteria in shaping an immune
response that mediates the balance between health and disease.
Unlocking how beneficial bacteria affect the development of the immune
system may lead to novel and natural therapies based on harnessing the
immunomodulatory properties of the microbiota.
PMID: 21034976
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21034976/?tool=pubmed
READ this AGAIN from that link:
http://7thspace.com/headlines/380215/the_human_gut_is_filled_with_100_trillion_symbiotic_bacteria.html
OK i WILL randall TAR baby...
And i'm sure you will READ it again NOW: LoL
[...] The human gut is filled with 100 trillion symbiotic bacteria—ten
times more microbial cells than our own cells—representing close to
one thousand different species. "And yet, if you were to eat a piece
of chicken with just a few Salmonella, your immune system would mount
a potent inflammatory response," says Sarkis K. Mazmanian, assistant
professor of biology at the California Institute of Technology
(Caltech).
Salmonella and its pathogenic bacterial kin don't look that much
different from the legion of bacteria in our gut that we blissfully
ignore, which raises the question: What decides whether we react or
don't? Researchers have pondered this paradox for decades.
In the case of a common "friendly" gut bacterium, Bacteroides
fragilis, Mazmanian and his colleagues have figured out the surprising
answer: "The decision is not made by us," he says. "It's made by the
bacteria. Since we are their home, they hold the key to our immune
system."
What's more, the bacteria enforce their "decision" by hijacking cells
of the immune system, say Mazmanian and his colleagues, who have
figured out the mechanism by which the bacteria accomplish this feat—
and revealed an explanation for how the immune system distinguishes
between beneficial and pathogenic organisms.
In addition, the work, described in the April 21 issue of Science
Express, "suggests that it's time to reconsider how we define self
versus non-self," Mazmanian says.
Like other commensal gut bacteria—those that provide nutrients and
other benefits to their hosts, without causing harm—B. fragilis was
thought to live within the interior of the gut (the lumen), and thus
far away from the immune system. "The dogma is that the immune system
doesn't respond to symbiotic bacteria because of immunological
ignorance," Mazmanian explains. "If we can't see them, we won't react
to them."
But using a technique called whole-mount confocal microscopy to study
the intestines of mice, he and his colleagues found that the bacteria
actually live in a unique ecological niche, deep within the crypts of
the colon, "and thus in intimate contact with the gut mucosal immune
system," he says.
"The closeness of this association highlights that an active
communication is occurring between the bacteria and their host," says
Caltech postdoctoral scholar June L. Round.
From that vantage point, the bacteria are able to orchestrate control
over the immune system—and, specifically, over the behavior of immune
cells known as regulatory T cells, or Treg cells. The normal function
of Treg cells is to prevent the immune system from reacting against
our own tissues, by shutting down certain immune responses; they
therefore prevent autoimmune reactions (which, when uncontrolled, can
lead to diseases such as multiple sclerosis, type 1 diabetes, lupus,
psoriasis, and Crohn's disease).
Bacteroides fragilis has evolved to produce a molecule that tricks the
immune system into activating Treg cells in the gut, but in this case,
Mazmanian says, "the purpose is to keep the cells from attacking the
bugs. Beautiful, right?"
In their Science paper, Mazmanian and colleagues describe the entire
molecular pathway that produces this effect. It starts with the
bacteria producing a complex sugar molecule called polysaccharide A
(PSA). PSA is sensed by particular receptors, known as Toll-like
receptors, on the surfaces of Treg cells, thus activating those cells
specifically. In response, Treg cells suppress yet another type of
cell, the T helper 17 (Th17) cells. Normally, Th17 cells induce pro-
inflammatory responses—those that would result, for example, in the
elimination of foreign bacteria or other pathogens from the body. By
shutting those cells down, B. fragilis gets a free pass to colonize
the gut. "Up until now, we have thought that triggering of Toll-like
receptors resulted solely in the induction of pathways that eliminate
bacteria," says Round. "However, our studies suggest that multiple yet
undiscovered host pathways allow us to coexist with our microbial
partners."
When Mazmanian and his colleagues blocked this mechanism—by removing
the PSA molecule, by removing the Toll-like receptor for PSA, or by
eliminating the Treg cells themselves—the bacteria were attacked by
the immune system and expelled. "They can no longer co-opt the immune
system into inducing an anti-inflammatory response, so the formerly
benign bacterium now looks like a pathogen," he says, "although the
bug itself is exactly the same."
"Our immune system arose in the face of commensal colonization and
thus likely evolved specialized molecules to recognize good bacteria,"
says Round. Mazmanian suspects that genetic mutations in these
pathways could be responsible for certain types of immune disorders,
including inflammatory bowel disease: "The question is, do patients
get sick because they are rejecting bacteria they shouldn't reject?"
On a more philosophical level, Mazmanian says, the findings suggest
that our concept of "self" should be broadened to include our many
trillions of microbial residents. "These bacteria live inside us for
our entire lives, and they've evolved to look and act like us, as part
of us," he says. "As far as our immune system is concerned, the
molecules made by gut bacteria should be tolerated similarly to our
own molecules. Except in this case, the bacteria 'teaches' us to
tolerate them, for both our benefit and theirs."
<snip>
June Round gets AROUND with Mazmanian:
5 hits:
"Mazmanian SK"[Author] round
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mazmanian%20SK%22%5BAuthor%5D%20round
I havent' posted these two:
#3 of 5
http://www.ncbi.nlm.nih.gov/pubmed/19963349
J Autoimmun. 2010 May;34(3):J220-5. Epub 2009 Dec 6.
Coordination of tolerogenic immune responses by the commensal
microbiota.
Round JL, O'Connell RM, Mazmanian SK.
Source
Division of Biology, California Institute of Technology, 1200 E.
California Blvd, Pasadena, CA, USA. jro...@caltech.edu
Abstract
All mammals are born ignorant to the existence of micro-organisms.
Soon after birth, however, every mammal begins a lifelong association
with a multitude of microbes that lay residence on the skin, mouth,
vaginal mucosa and gastrointestinal (GI) tract. Approximately 500-1000
different species of microbes have highly evolved to occupy these
bodily niches, with the highest density and diversity occurring within
the intestine. These organisms play a vital role in mammalian nutrient
breakdown and provide resistance to colonization by pathogenic micro-
organisms. More recently, however, studies have demonstrated that the
microbiota can have a profound and long-lasting effect on the
development of our immune system both inside and outside the
intestine. While our immune system has evolved to recognize and
eradicate foreign entities, it tolerates the symbiotic micro-organisms
of the intestine. How and why this tolerance occurs has remained
unclear. Here we present evidence that the commensal microbes of the
intestine actively induce tolerant responses from the host that
coordinate healthy immune responses. Potentially, disruption of this
dialogue between the host and microbe can lead to the development of
autoimmune diseases such as inflammatory bowel disease (IBD),
rheumatoid arthritis (RA), or Type I diabetes (TID). As a wealth of
publications have focused on the impact of the microbiota on
intestinal immune responses and IBD, this chapter will focus on the
extra-intestinal impacts of the microbiota from development to disease
and integrate the known mechanisms by which the microbiota is able to
actively communicate with its host to promote health.
PMID: 19963349
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19963349/?tool=pubmed
#4 of 5
http://www.ncbi.nlm.nih.gov/pubmed/19343057
The gut microbiota shapes intestinal immune responses during health
and disease.
Round JL, Mazmanian SK.
Nat Rev Immunol. 2009 May;9(5):313-23. Review. Erratum in: Nat Rev
Immunol. 2009 Aug;9(8):600.
PMID: 19343057
^^^^^^^^^^^^^^^^^^^^^^
And we have 26 hits for MUC1 in the group as of today:
muc1 - 26 hits - P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=muc1&start=0&
ONLY 3 of these 26 have iron... till today of course:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=muc1+iron+&start=0&
ONLY 47 muc1 + iron in ALL groups:
http://groups.google.com/groups/search?qt_s=1&q=muc1+iron+
And a clue from one of them takes me HERE:]
http://www.cancer.gov/cancertopics/pdq/cam/laetrile/HealthProfessional/page4
[...] In the fourth study, cultured human bladder cancer cells were
treated with amygdalin alone or a combination of amygdalin and an
antibody that was coupled (chemically) to beta-glucosidase.[20] The
target for this antibody was the glycoprotein (a protein with sugar
molecules attached) MUC1. Aberrant forms of MUC1 are produced and
displayed at high levels on the outside of several types of cancer
cells, including bladder cancer cells. In this study, amygdalin alone
was not very effective in killing the bladder cancer cells, but its
cell-killing ability was 36 times greater in the presence of the
antibody-enzyme complex. There are two possible explanations for this
increase in cell-killing ability. The first is that antibody-enzyme
complexes bound via MUC1 produce high rates of amygdalin breakdown at
the cell surface. This breakdown leads to high local production of
cyanide, which is quickly taken up by the cells and kills them. The
second explanation is that antibody-enzyme complexes bound to the
cells are internalized, thereby increasing the intracellular
concentration of beta-glucosidase. Increased beta-glucosidase activity
inside a cell would result in increased breakdown of amygdalin taken
up by it, and increased cyanide production and cell death. These two
potential mechanisms are not mutually exclusive. In another
experiment, the researchers cultured bladder cancer cells in the
presence of human brain tumor cells, which do not express MUC1. When
this coculture was treated with amygdalin and the antibody-enzyme
complex, the bladder cancer cells were killed selectively. In view of
the mechanisms proposed above, this result is not surprising, since
the bladder cancer cells and the brain tumor cells in this coculture
formed homogeneous colonies (colonies that contained exclusively
bladder cancer cells or brain tumor cells). Conceivably, selective
killing of some types of human cancer cells might be achievable
through application of this method; however, these positive results
must be confirmed independently, and the effectiveness of this
approach in animal models must be demonstrated before its use in
humans can be considered.
<snip>
Eat soybeans and take a chill pill?
http://www.ncbi.nlm.nih.gov/pubmed/21593350
Soy protein diet, but not Lactobacillus rhamnosus GG, decreases
mucin-1, trefoil factor-3, and tumor necrosis factor-α in colon of
dextran sodium sulfate-treated C57BL/6 mice.
Jiang H, Przybyszewski J, Mitra D, Becker C, Brehm-Stecher B,
Tentinger A, MacDonald RS.
J Nutr. 2011 Jul;141(7):1239-46. Epub 2011 May 18.
PMID: 21593350
^^^^^^^^^^^^^^^^^^^^^^^^
Little-Known Secrets about Optimal Iron Levels
Posted By Dr. Mercola | July 14 2009
http://articles.mercola.com/sites/articles/archive/2009/07/14/Little-Known-Secrets-about-Optimal-Iron-Levels.aspx
[...] mercola -Is Iron Helping or Slowly Killing You?
http://www.youtube.com/watch?v=g8pQsH7c1sc
<time: 8:44> <views: 3,675>
=================
Build uP GpX and SOD via Glutathione and NAC supplements:
http://www.whale.to/vaccine/tylenol_depletes_glutathione.html
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
randall... i better get some eXXXercise... now... i want HIGHer IRON
(Fe) levels to be strongER
Bohgosity BumaskiL
May 27, 2012, 1:13:48 AM5/27/12
to
On 2012-04-09 4:11 PM, randall wrote:
> Randall quoted:
I don't like this article's major source of Iron (red meat). You can
get plenty of Iron from Beets, Spinach, and Tomatoes, especially if
you complement them with some Vitamin C in citrus fruit. My problem
with the red meat theory of major iron sources iz that it
contributes to the article's main target; obesity.
The best cancer vaccine iz prevention. Your body, az evidenced by
this dizeaz called psoriasis is plenty capable of attacking
corruption of itself; cancer. The object of psoriasis treatment iz
jenerally turning down that auto-immune response, preferably by
reducing factors of self-corruption.
> Randall quoted:
> http://www.wellnessresources.com/weight/articles/stunning_discoveries_regarding_iron_obesity_candida_thyroid/
> Stunning Discoveries Regarding Iron, Obesity, Candida & Thyroid
> > (...)
> Stunning Discoveries Regarding Iron, Obesity, Candida & Thyroid
> > Adequate iron intake (red meat) compared to obvious iron loss
> > (menstrual cycles, etc.) is still important to understand.
> > (...)
> > (menstrual cycles, etc.) is still important to understand.
I don't like this article's major source of Iron (red meat). You can
get plenty of Iron from Beets, Spinach, and Tomatoes, especially if
you complement them with some Vitamin C in citrus fruit. My problem
with the red meat theory of major iron sources iz that it
contributes to the article's main target; obesity.
The best cancer vaccine iz prevention. Your body, az evidenced by
this dizeaz called psoriasis is plenty capable of attacking
corruption of itself; cancer. The object of psoriasis treatment iz
jenerally turning down that auto-immune response, preferably by
reducing factors of self-corruption.
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